Test #1 Flashcards

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1
Q

Misconception about Darwin

A

The importance of Darwin himself – people think that only he came up with theory or that all scientists were against him and he revolutionized the idea –> NOT TRUE
- Misconception = that he came up with his ideas suddenly all on hos own –> In reality – his grand idea didn’t come about in a vaccum

***Darwin was just in the right place at the right time to get the credit BUT he was not the only person

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2
Q

What led Darwin to his ideas (overall)

A

He was alive at the point of intersection of intellectual processes that led people towards this direction

***NOTE: He was NOT the only person to connect the dots at the time of connection

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3
Q

Darwins concluions were…

A

An inevitable outcome of broader perspectives at the time – the reason that he gets too much credit (it wasn’t as revolutionary as people make it seem)

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4
Q

Persectives in the past (limitations on people)

A

At Darwins time – it was hard to have sufficient perspectives for one person –> Took time to draw out that perscteive to think about areas that you weren’t around

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5
Q

Understanding Earth’s age

A

Took time to know that earth is older than what we know –> hard to get that persective

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6
Q

Importance of Empirical Thought

A

Once scientific empirical thought took hold = increased understanding of earth iteself –> THEN applies this to biological systems

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7
Q

Who set the stage for Darwin’s profound realization

A
  1. Nicholas Steno
  2. William Smith
  3. James Hutton + Charles Lyell
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8
Q

Darwin (Overall)

A

Great Naturalist

***He travelled = gave him first hand persective on the variety of the world + how wide the world was

***His ideas did NOT come about in a vacuum

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9
Q

How did Darwin draw his conlusions

A

Drew conclusions from years of observations of species in their natural envirnments + Fossils + patterns of traits in domesticated animals
- He had first hand expriences of variety of world + how wide the world was from travelling

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10
Q

Key Developments before Darwin

A
  1. Antiquity of the world
  2. The relationships among organisms
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11
Q

Nicholas Steno

A

Overall: Established the underlying Premise of geology
- Dutch Bishop
- First real academic realization of what FOSSILS are

Example – Shark Teeth – before they didn’t connect that they came from living things
- Notes distirbution of fossil marine animals in terrestial rocks
- Developed idea of straigraohy
- Was only looking at local rocks
- had understanding of geology –> understood that we can study earth via studying rocks

***made a system to study rocks within his region

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12
Q

Stratigraphy

A

Study of the layers of rocks in terms of chronology
***Idea was developed by Nicholas Steno

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13
Q

Steno + Stratigraphy

A

He developed idea of straigraohy – he found that the laters reprented chronology – that diffrent layers are diffrent events in geologic history

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14
Q

William Smith

A

English Surveyer

Overall: Was able to see the big picture of stratigraphy – connected rock formation in diffreent parts of Britain –> Aligned rocks in one area to rock layer in a different areas based on fossils (found the same types of fossils in layers but in diffreent places = knew they had to be from the same time)
- Notes that the strata from across england showed remarlable consistencey in the fossils that they hold
- Found strata can be identofied across wide geographic span by “index fossils”
- Broadened Stratography – NOW not just in one place
- Understood earth on larger scale
***Did his work because looking for mines

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15
Q

Index fossils

A

Fossils that serve as diagnostics for a particular geologic period
***Index fossils = indicate layer

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16
Q

What did Smith see?

A

He connected rock formation in diffrent parts of Britain –> Aligned rocks in one area to rocks in layer in different area – saw the same change over time
- Saw that particular layers of rock in different parts of the world can be aligned by fossils in the layers

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17
Q

James Hutton + charles Lyell

A

Overall: Found that processes that have built and shaped geologic strata are essentially the same as the processes we see at work today
- Understanding geologic processes NOT just patterns anymore

Suggested: that the grdaual nature of these porcesses indicates that earth MUST be expreml;ey old
- Thought about porcesses happening today and how they scale over time to create what we see
- Understood what happened in Past + When we scale up rate of ongoing processes wbnough to see large scale processes we see – wouold mean that earth need to be much older than people thought before

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18
Q

What came from Hutton + Lyell

A

Created Uniformitarism

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19
Q

Uniformitarism

A

Natural Laws observable around us now are also responsible for events of the past
- Means that the properties of the universe have not foundationally changed over time –> Same processes for history of earth.
- Means that the same laws of nature are not changing from expeirmnet to expeimnet
**Idea that the present is the key to the past
**
Really important in science
***Came out of geology

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20
Q

Why is Uniformitarism important in scinece?

A

Because it means that the same laws of nature are NOT changing from experiment to experiment – very important in science

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21
Q

Things in geology that affected biology perspective

A
  1. Found that the earth is old
  2. Makes sense of broadening persiectives
  3. Explains things by sclaing up ongoing processes – don’t need supernatural explinations for things
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22
Q

Relationships among organisms (overall)

A

Broader view of the living worls arts to take shape around that time – it took leaving small town to broaden persepctive

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23
Q

Linneus

A

Overall: father of taxonomy + binomial nomenclature – made hiearch –> Tied together all we know about life forms
- Gave comprehensive volume for how living world is connected
- Classified and named over 12,000 species of plants and animals
- Searched for divine plan in relationship among taxa
- Though species are immutable (Do not change) – BUT he still found connction between them
- Found connections between living things
- Set ground of perscetive for people to make DWM

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24
Q

Buffon

A

Naturalist – started grappeling with ohysical mechanistic explinations of the earth and living world long before Darwin

OVERALL: recoignized the improtnace of patterns in biogeography
- Observing regional differnces among species led some to start thinkning that species might not be immutable
- one of the first naturalists to begin expressing teh ideas that species may change over time
- Paying attentoon to differnece between organisms of the same species
- Thought about the idea that species change through time

Question: How did differences come about – does it show that organisms change across space

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25
Q

Biogeography

A

The study of distribution of species across space – observing regional diffreences among species led some to start thinkning that species might not be immutable

Example:
1. Wolves – North America/Siber = Large Vs. tropical = Small

  1. Moose – Alaska Vs. Scandanavia
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26
Q

Buffon realization

A

Thought about the idea that species change through time – did it by how species are distributed across the world –> Disrubution might tell us about how organisms might change

Question: How did differences come about – does it show that organisms change across space

***Shows that the idea of species changing over time did not start with Darwin

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27
Q

Buffon Ideas

A

Thiought all soecies were made in Europe and then they dispersed and degraded

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28
Q

Lamarck

A

Overall: Described how traits of organisms are matched to their envirnments and habitats
- Said traits of organisms match their envirnments well –> came up with how organisms change over time + how change is tramitted thorugh time
- Thought species change over time
- First to develope a cohesive thory in how organisms evolove
***Came up with 1st theory of how heredity works BUT he was wrong

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29
Q

Lamark’s heredity

A

Said that traits of organisms match the envirnment well –> came up with how organisms chnage over time + how chnage is transmitted through time

HAD IDEA OF AQUIRED INHERTIANCE

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30
Q

Who was the ifrst to develope a cohesive thoery in how irganisms evolove?

A

Lamark

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31
Q

Lamarkism

A

Change in organisms brought by natural physical processes

Contains:
1. Force of coplefications (Spontenous generation) – increase in complexity through time
1. Force of adaptations (Aquired inheritance) – match body to envirnment – idea of how organisms chang over time

Example – Giraffes necks get longer
***Had idea of aquired inheritance

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32
Q

Cuvier

A

Father of paleontology from a biological persective – put fossils in biological context

Geeatest contirbution – realuzation of excitcion – credited with deomnstrating that extiction is real
- realized that geologic history was charachterized by waves of diffrent fauna
- Still thought species were immutable
- Thought ecosystems are created and destroyed over again

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33
Q

Cuvier ideas

A

Idea of catastophism – thought that ecosystems are created and destroyed over and over again

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34
Q

How did Dawrin make observations

A

Restless young man – joined the company of naval vessel at 22 00> circumnavigated the globe – giving breadth of perscetive on nagural world that few with his interstes and training experinced

***Because of this = he made observations of living and geologic world

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35
Q

Darwin’s observation in context

A

He was making these observations about the worlkd in the intelecual context

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36
Q

Inevitability of Darwin’s conclusions

A

His ocnclusions were inevitable – this view of life was coming into focus anyway
- He was NOT the only person with ideas at the time

Dawrin was thw the first person to put all of the peices together BUT he sat on his ideas for a decade
***We give darwin too much credit – it was inevitable conversion of intersection

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37
Q

How do we know that Darwin’s conclusion were inevtiable

A

Becayse Wallace had independelet arrived at the same conlsuions – shows that the conclsuions were inevitable because it actuallt did happen somegere else

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38
Q

Wallace

A

He came up with the same conclsuoons as Dawrin independeley – he was more eager to announce his finidngs= spurred Darwin to publish his work

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39
Q

Dawrin + Wallace

A

came up with same conclsuions – wallace was more eager to announce his findings = spurred Darwin to publish his work –> Darwin gets credut becayse he was rocher

***Shows influence of class politics

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40
Q

Componenets of Darwinian Evolution

A
  1. Pattern
  2. process
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41
Q

Pattern of Darwinian Evolution

A

Common decent – Descent with modification

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42
Q

Process of Darwinian Evolution

A

Mechanisms for how changes arrive – process = natrual selection

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43
Q

Which is more acceoted pattern or processes

A

People NOW accept natural selection (process) more than the pattern
- The common decent thing is the thing that people don’t like

AT Darwins time it was the opposite – people didn’t accept the mechanism

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44
Q

Why didn’t people accept mechanism at Darwin’s time?

A
  1. They didn’t have the math to show the mechanism at the time
  2. They didn’t have the genetic idea at the time – didn’t know about heredity
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45
Q

Two models for explaining patterns of biodiversity

A
  1. Special Creation
  2. Descent with Modification
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46
Q

Modern science

A

Essnetially we are confronting models with data to disprove models

Example – comparing models of special creation with DWM

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47
Q

Special Creation

A
  1. Species are immutable (unchnaging)
  2. Lneages fo NOt diverge
  3. Species are created seperatley
  4. Species are geniologically independet – not fundementally realted to each other
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48
Q

How did they combine special creation + fossils

A

There was an idea that all things were created at one point and existed over time

***They didn’t really think that this was true because they knew extictions happen because of fossils = they thought that species are made at once and then die and a new species is made

Overall: idea that species pop in and out of existence

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49
Q

Descent with Modification (overall)

A
  1. Species change thorugh time
  2. Single lineases give rise to many – diverge
  3. Old forms beget new forms – connects round history of life –> genologically realted
  4. Species are geniologically related
  5. Requries the earth to be vastly older than recorded human history – requires a huge amount of time for this to occur
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50
Q

Lines of evidence for Descent with Modification

A
  1. Do species change over time
  2. Does special occur?
  3. Do new forms arise from old?
  4. Are different Groups of organisms related
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51
Q

Do species change over time OR are they fixed in traits?

A

We know that species change over time because we can make them change – we domestricate things = we chaneg theor traits over time = we know that their can change

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52
Q

How do we make species change

A

We domesticate things = we know that species change over time

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53
Q

Evidence of species changing over time

A
  1. Artifcial Selection
  2. Applied Breeding (domestication)
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54
Q

Evidence for populations changing undeer human control

A

Artifical selection – seen in scientific experiments –> shows species change over time
- Can see change in behavioer
- String interfences
- Often modest expected change
- experiments can also involove exposing popularions to experimental conditions and measuring for heretible change

Example – do experimnet with mice runing on treadmill – only take the fastest mice and breed them

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55
Q

Agents of selection in selection experiment

A

Humans – if doing selection experiment = people impose selection –> humans are the agents of selection

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56
Q

Second type of experiment that shows species change over time

A

Experimental evolution –> expose populations to experimental conditions and measure for heretible chnages

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57
Q

Experimental evolution

A

Take population and expose to new conditions – see change

***SHows that species change over time

Example – Threespine sickle back

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58
Q

Threespine sickle back experimnet

A

Overall: Taking population and exposing to new conditions to see change

Threespine sickback = occurs in marine and freshwater popultions
- The freshwater popultions = have better cold tolerance
- When take diffreent popultions from nature and carfully test the thermo tolerance in lab reared genertaion THEN tranfer them to expeirmntal ponds with cold conditions
- DOES NOT have acrtive control breeding – not purposfully putting the cold tolerant fish with cold tolerant fish

Result: When bring them back into the lab and have offspring under contrlled conditions –> the offsrping cold tiolerance imporved by 2.5 degrees in just 3 generattions – minimum temperature of gish improves –> now they can maintain homeostatsis in coldeer envirnment
- exposure to colder –> have phenotypic shift
- NOT picking only the cold tolerant – all of them can made

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59
Q

Applied Breeding

A

Domestication – shows that species change over time

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60
Q

Morphological change in applied breeding

A

Applied breeding = shwos there can be morphological chnage (physical chnage – change to body structure)

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61
Q

History of Applied breeding

A

We have a long history of selevctive breeding fo domestic plants + Animals giving rise to unambiguous answer that species DO change over time

Example #1 – Dogs – share common ancestory
- Wolf = common ancestory –> have morphological shift becased on humans applying selective pressure (getting different breed of dogs)
- Morphologic change can be seen in cranium
- Would say that they are different species beased on morphology if you didn;t know that they were all one

Example #2 – Can be seen in plants (we domesticate plants too = we know species change over time) –> Wild mustard
- The common wild mustard plant was domestricated to make many plants –> all domestirca forms of same common ancestral plant

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62
Q

Does speciation occur?

A

ANSWER: YES – many expamples of recent on-going speciation in nature

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63
Q

Speciation

A

One lineage splits into two seperate lineages

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64
Q

Do new forms arise from old?

A

YES
Evidence:
1. Biogeographhical + paleotological evidence –> Seen in law of sucession
2. Transitional Fossils

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65
Q

What connects organisms across history of life?

A

Old forms giving rise to new forms

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66
Q

Law of Succession

A

Correspondance among fossils and existing faina dn flora in spaces
***Evidence that do forms arise from old
- Correspondance across modern organisms and possible origins in the same space –> Modern organisms in a space corresponds to the fossils in that space

Example #1 – Australian fossils that are mammals are marsupials BUT asiam mammals are placentals

Example #2 – Apes – see modern and fossils in the same place

Example #3 – Sloths –> they are ONLY found in the new world – connects modern fossils in the same regions

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67
Q

Wallace Line

A

Differentates faina of asian origin with fiana of australian origin
- Seperates placentals Vs. Marsupials

***Seen in fossils + existing organisms

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68
Q

What do we expect to see in the fossil record IF new forms arise from old?

A

Exoect to see fossils with mixes of Ancestral and Novel traits

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69
Q

Transitional Fossils

A

Fossils with mix of ancestral and novel traits – ties groups of organisms over time

Example – Dinasours with feathers

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70
Q

Misconception about Transitional Fossils

A

That they are link between two things

Transitional Fossils are NOT link between two things – they are a branching point with a mix of traits
- they are NOT direct loinks rather they are reprenstative of organisms that shared a common ancestor with a group near a branching point

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71
Q

Predictions about transitional fossils

A

Based on gaps between existing organisms and ones in the fossil record = we can make predictions about what transitional form to expect
- In some cases paleotologists have been very sucessful with this

Example – evolution of whales

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72
Q

Evolution of Whales

A

Whales = hoof mammals
- Evolution of whales from terrestrial ungulates in the Eocene to Ocean going + Krill feeding giants of today
- once found where to look = found the set of transition fossils to connect the dots

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73
Q

Connectivity in the living world

A

IS NOT along a single tradectory – NOT a straight line
- People think that evolution is a single tradjectory – that it is a direct progression within a single lineage over time –> NOT TRUE

EVOLUTION – is NOT a singloe lineage – have branching diversification over time = need to contextulaize thorugh fossils

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74
Q

Example of Transitional Fossils

A

Whales – conects 2 kinds of hippos and 2 kinds of whales

Start = mammal – know many steps occur in trantion
- Can see fossils with hind limbs –> orginals that ahve all BUT one feature
- Orginal mammal = not direct ancsetor BUT is part of the processes
- Can see existing organisms with lens
- Example transitional form = filter feeder + some no teeth
- Still living organisms can be transitional forms
***Transitional forms shows mix of trauts that allows us to understand developement

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75
Q

Homology

A

Charachteristics shared among orgnaisms because they were inherited from a common ancestory
***homolgous traits
- Similarities = biologically meaningful NOT just coincidence – they are because of a common ancestor

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76
Q

Example of homology

A
  1. Mammal Limb Bones
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77
Q

Evidence that different groups of organisms are related

A
  1. Homology
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78
Q

Mammal Limb bones

A

Limbs = highly conserved –> ecen if they are in diffrent shapes and sizes and have different purposes

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79
Q

Better Forms of homolgous traits

A

There are better forms for homolgous traits for their function BUT they are confined by shape in ancestory

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80
Q

Places homology is seen

A
  1. Vestigal traits
  2. Atavism
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81
Q

Vestigal Structure

A

A useless rudimentary version of a trait that is a function in related taxa
- Reminent of traits in ancestors

Example
1. Psudgogenes
2. Moden Whales
3. Appendix

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82
Q

Psudogenes

A

Non-functional copies of coding genes

Example – Vitamen C synthesis in Primates
- Humans need to ingest vitaman C BUT other animals don’t –> this is because hour ancestors were furgavors = they were not limited in vitamn C –> there was a mutation that stopped vitamen C. production BUT there was no bad effect because we got enough Vitamen C in diet = kept mutation

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83
Q

Whales + Vestigal traits

A

Modern whales = have no hind limbs BUT they have a pelvis bone that is not attatched to anything because ancestors had hind limbs

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84
Q

Appendix + Vestigal trait

A

Appendix = was thought to have NO use BUT now we think it may play some role in gut microbiome

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85
Q

Atavistic Traits

A

Reappearnce of ancestral traits in individuals
- Provised evidence of homology in developmental pathways

Example – more than 2 nipples

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86
Q

Use of Atavistic traits

A

Provide evidence of homology in developmental oathways – mutation in development occurs that re-turns on a gene

***We can manipulate atavistic traits ourselves

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87
Q

Manupulating Atavistic traits

A

We can manipulate appearnace of atavistic traits – can exeperimentally trun on latent homolgous developmental pathways

 - Evo-Devo + evidence for homlogy in developmental pathways -- look at how ancestral pathways work 

Example – make chicken that can grow teeth

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88
Q

Patterns of homology

A

Describe relationships among taxa –> Because homology is based on common ancestry it leads to specific nested patterns of traits among relation organisms

***Makes nested patterns of traits among organsims
- Nested rather than Vendiagram
- nested with each other
- Nested in the same sense as the standrad taxonomic hiearchy – refected in classifciation system

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89
Q

Where else can homology be seen

A

Have homology in DNA and protein sequences

***have the same nesting sturcture in genetics as we do in traits –> Genologic nesting

Have:
1. Orthologs
2. paralogs

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90
Q

Orthologs

A

Homolgous genes between species – across species

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91
Q

Paralogs

A

Homlogous genes that diverged within a lineage
***genologics relate to each other within sme species
- Genes related within ONE genome

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92
Q

What makes paralogs

A

Paralogs = result of gene duplication events – genologics related
- Gene + chromosome + Whole genome duplication event

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93
Q

What forms the basis for modern phylogentics

A

Orthologs + Paralogs – genologics related to eachother

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94
Q

Example recent gene duplication

A

A recent duplication of DNA sequences around nueron gene PMP22
***makes PMP-22 flanked on both sides by CMT1A repeat

  - RT repeats that flanks = can be bad --> can end up losing a copy or end up with two during recombination 
   - Nearby repeates make the region prone to mitotic probelms 
- Erroes in duplciation can lead to disease
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95
Q

Charcot-Marie tooth diease

A

Errors in duplication in PMP22 because of RT repeats that flank both sides
***loss of genes = get disease

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96
Q

When did duplication event in PMP-22 occur?

A

Occured sometimes bteween most recent common ancestor of homo + pan + gorllia and most recent common ancestor of homo and pan
***Repeat is found in homo + pan
- Pan = chimps + babones
- Humans + Chimps + Baboes = have copies

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97
Q

Why are PMP-22 repeate NOT convergent evolution

A

NOT convergent evolution because the traits are NOT adaptive

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98
Q

Why are PMP-22 repeate NOT convergent evolution

A

NOT convergent evolution because the traits are NOT adaptive

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99
Q

Two broad compoenents of Darwin’s ideas

A
  1. pattern – common Descent
  2. Process – mechanisms for how change arises over time –> process that generates diversity + process that connects diversity
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100
Q

Two overall changes that led to Darwin’s ideas

A
  1. Change in geologic thought
  2. Change in biologic thought

BOTH led to Darwin’s ideas on pattern

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101
Q

Intelecual setting for Darwin’s breakthroughts

A
  1. Break through on pattern in Geology (led to pattern)
  2. Breakthrough on pattern in biology (led to pattern)
  3. Breakthrough on Process – Malthus (led to process)
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102
Q

Malthus affect

A

Affected both Darwin + Wallace (Darwin + Wallace both read his work)
- Gave breakthrough to figure out process – mechanism for how change arises over time

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103
Q

Malthus (overall)

A

Was one of the first people to really think about teh mathamatic reality of human demography
- We would now call what he did “demography”
- he put numbers to issues of human populations – made many models
- He realized the remarkable power of unchecked population growth

***At the time people were thinking about mathamatic models for population growth

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104
Q

Demography

A

The study of population structure

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105
Q

Importance of Malthus

A

His line of thought was critical fro Darwin + Wallace idea of natural selection as the mechanism of change
- critical for coming up with MECHANISM

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106
Q

What did Malthus find?

A

He realized the remarkable numerical power of unchecked population growth
- Realized math potential in how reproduction oppertates that makes population growth unstable process

Showed that the way popultions grow through time = leads to massive growth UNLESS it is in check

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107
Q

Malthus opinion on population growth

A

He viewed this intrinsic property of populations (that unkecked growth) as a source of great human sufferering

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108
Q

What did Malthus finding show?

A

Means that something needs to hold population growth back – without check the population is unstable and unsustainable

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109
Q

Geometric/Exponential growth

A

Population is increasing by constant rate per individual over time

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110
Q

Geometric Vs. Exponetial growth

A

Geometric = discrete units of time
Exponential = continous time

***Difference between the two = how you keep track of time (discrete vs. continous time)

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111
Q

Arithmetic growth

A

Population increase by a constant amount over time
- Increase by a constant amount of individuals

***Different than versions where you add individuals based on the density of the popultion – this does not take into account the density of the population

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112
Q

Two types of growth

A
  1. Arithmetic
  2. Geometric/exponential
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113
Q

Arithmetic growth equation

A

Yt = Yo + XT –> JUST a linear equation

T = time
Overall – Number of individuals X Time (because adding the same number of individuals each time no matter how big or small popultion is)
- Each generation as set number (X) individuals added to the populton

Example – start with 1 person and add 2 people each generation
1 –> 3 –> 5 –> 7 –> 9
- Adding a fixed number each time

***Creates linear popultion growth (Always adding 2 individuals each time)

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114
Q

Exponentailo growth equation

A

Yt = Yo X X^t – for each generation t -> X offspring PER individual are added
- Adding X offspring per individual (Y)

Example – start with 1 individual and the popultion grows at a rate of 2 individuals per generation

1 –> 2 –> 4 –> 8 –> 16

***Much more rapid growth than arithmetic model

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115
Q

What type of growth is seen in popultions

A

Most is exponental growth –> seen in almost all real popultions in nature
- Seen by looking at reproduction

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116
Q

What type of growth did Malthus notice

A

Exponential growth – he notives this because we are NOT actually in an exponental model = means that there is some outside force that needs to be occuring

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117
Q

Who is included in growth models

A

We only look at growth from the persective of females –> THEN once do equations add back in males
- only look at females + female offspring
- Then you can apply the sex ratio for a given popultion (often assume 50:50) –> THEN can add males back in

Example – if in the end you calculate 32 indivudals THAT means 32 females –> Assuming 50:50 ratio - means your total popultion is 64 (32 + 32)

***Works IF we know things about the sex ratio

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118
Q

Malthus equations (image)

A
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119
Q

Fibonachi

A

Came up with sequnce to try and come up with a model for popultion growth – it was an attempt to put numbers to popultion before malthus

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120
Q

What did Malthus realize

A

He considered exponential growth from the perspective of human popultions and agrucultural surplus – he realized that growth was a BIG problem for humans

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121
Q

Malthus + agriculture

A

He realized that exponential growth was a BIG probelm for humans – what would it do to agruculture?

Asked if we could save up resources to suppert humans

Answer: NO – human technology can’t keep pace if going unchecked = he thought that we were always on the edge of catastrophe
- Mortality would be higher if growth rates go unchecked
- Even with increases in production – agriculturakl surpluses would still inevitably lead to famine

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122
Q

What stops us from being in a state of catastrophe

A

Mortaloty rates stop us from being in a state of catastrophe
- High mortality rates stops catastrophe – most individuals due before reproduction in order for popultions to stay stable
- What prevents us = high level of background morlatlities to counterect popultions from rapid exponetial growth

***If most don’t survive = more stable popultion

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123
Q

Does growth models hodl true for most animal popultions

A

YES – numbers held true for most animal popultions – also found that mortaloity is a fundemental property of most popultions

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124
Q

What explains constant growth (what explains ability to mainatin expo growth model and not be unstable)

A

Variation in survival + reprduction

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125
Q

Mathlthuianism + Darwin

A

In natural popultions and humans (at the time) most individuals born into the popultion don’t actually contribute to the next generation

***This view of a struggle for existance as intrinsic to all popultions = critical to the formation of Darwin;s ideas for a mechanism

***Because most of popultion isn’t surviving –> means there is a variation in success = got Darwin + Wallace thinking

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126
Q

Uniquness of Darwin’s mechanism

A

The idea of the mechansim was not completley unique –> the importance of Darwin’s work was in coupling the process with the pattern
- Widening the scope of selection to encompess all of the loiving world

STILL – he wasn’t the only one to come up with his conlcuoon –> wallace came up with the same idea – spurred Darwin to finally publish

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127
Q

Importance of Darwin

A

Coupling the process + Pattern

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128
Q

Orginal Word Model of NS

A

Based on 4 tesable posutalates
- Built on a set of 4 postulates that are testable to epxlain data

***All postulates are testable

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129
Q

Why did natural selection remain controversial

A

Because Biology and Math had to catch up

  1. We didn’t have a mechanism for inheritance –> hard to prove
    • Mendle have us some idea –> use it for small traits BUT coupling mechansism of inheritance for complex variation too time to build understanding
  2. Anylzying variation in popultions – ststistics
    • Answer to many probelms
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130
Q

What was more accpeted for darwin + wallace

A

The pattern was accepted by scientofic community + public within 10 years BUT the mechansim of natural selection was controversial for longer
- Mechanism of natural selection was not accepted for another 50 years
- Mechansim remained controversial because testing is hard to do

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131
Q

NS postulates

A

NS is simple due to 4 key postulates

***Each postulate is testable BUT tesing is not always easy

  1. Populations are variable – variation within populations
  2. Traits are heretible
  3. Variation in survivorship + reproductive sucess
  4. Surivivorship + reproductive success vary as a function of traits
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132
Q

Postulate #1 – Populations are varaible

A

Populations differ in:
1. Morphology – body shape + Size + Structure
2. Color (ex. Sgells of snails)
3. Physiology (Ex. Cold tolerance + metabolic variation)
4. behavior
5. Life history traits (Ex. Growth + development + number of offspring/gametes)
6. Immunity (Ex. being resistant to disease + pathogens)

***This is fairly intuative – easy to see
- Certainly seen in human populations (Ex. Distrubution of height – math shows amount of variation)

***Can see how selection drives varaition

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133
Q

Where can variation be seen?

A
  1. Seen in human popultions – Example is disribution of height (math shows the amount of variation)
  2. See genetic variation within popultion – can see varaition in genome
    Example – HMHC antiogen protein in immune system
    • Gene in MHC = has over 1,000-2,000 allleles in human popultion

***Have varaition in physical (in phenotype) + vaiation in allele in genome

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134
Q

What is the hardest postulate to test

A

Postutlae #2 – traits are heretible

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135
Q

What do we mean in posulate #2 – traits are heretible

A

NOW we know about genetics BUT here we mean about heritablity = LOOKS across generation

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136
Q

Heretibility

A

Means that there is some connection between the phenotypes of one generation and the next
***Means that the offspring will look like the parents

 - Means that there a function in offspring that is in the parents 
  - makes many connections between phenotypes in offspring and parents 

***Very hard to demonstrate/show

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137
Q

What do we mean by “traits are heretible”

A

If we think in discrete generations – what we mean is simply that the phenotypic distribuition of generation 2 is at least partially a function of the phenotypoic distribution of their parents

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138
Q

Complexity of heretiability

A

Heretabiloity = rather complex in practice

***A trait can have a clear genetic basis BUT not be heretible in a straight foward way at the popultion level

Example – Genetic dominence –> NOT negating heritability BUT comlicats it

***Means that the second generation looking like their parents is more complicated than “just looking the same” – because of complex heritability patterns

***Traits can be heretible BUT not in a straight foward mechanism
Example – dominence –> complicates the 1:1 parent phenotype:offspring phenotype
- complicates the fact that the next generation will look exactley like the parents

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139
Q

Why is postulate #2 hard to measure?

A

Because heretibility is complicated

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140
Q

Example of heretibility

A
  1. Look at heights – looks at the children/sibling heights vs. the average height of both parents
    • Can see the mathamatic connection
    • Explains genes
    • Fits statistically significant line in parents vs. offspring
    • Hard to do things to contril for envirnment variation
  2. Mesuring beak size in parents vs. offspring
    • The relationship between the two could be because of genetics OR could be because of shared envirnmental factors
    • En
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141
Q

Second reason why is it hard to test heretibility

A

Because envirnmental factors affect traits – the correltion between parents and offspring could be because of shared envirnment

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142
Q

Second reason why is it hard to test heretibility

A

Because envirnmental factors affect traits – the correltion between parents and offspring could be because of shared envirnment

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143
Q

Postulate #3 – variation in survivorship + reproductive sucess

A

***Very easy to see + testable

***This postulate is almost universally true in natural popultions

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144
Q

Exceptions to Posutlate #3

A

Cases where a popultion is in the midst of exponetal growth

***When it isn’t true it is transient – only occurs for a few generations

Example of times when not true:
1. Invasive species – if colonizing a new habitat = grow rapidly until it hits its limits
2. If bounding back from an epidemic

***The rapid growth does not last for long –> if it did it would become overrun with organisms – means that almost ALL of the time you can check off postualte #3

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145
Q

Example of popultion in exponetial growth

A

Hex crane – we started conserving them to ensure their survival –> they are in exponential growth pahse while they are getting higher BUT they are only able to do this because people are ensuring their survival
- Won’t last forever

Example where postualte #3 is not true

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146
Q

What types of popultions does Postulate #3 work for?

A

Works for R and K stradegy populations

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147
Q

R stadegy

A

Investment optimized to the number of offspring – faster replication = put more babies hoping to survive

Example – octopus

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148
Q

Example R stradegy

A

Octupus –> makes 0.25 million ocotopi each generation
- replication rate = 125,000 (for females only – 250,000/2)
- Each octopuc gets pretty large

***If they were in exposnetial growth and all octopus survive to reproduce (meaning there is no variation in surivival + reproductive sucess) THEN by generation 4-5 the octopu would exceed the mass of the earth
- This is the reason why differential survival + reproduction needs to be true

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149
Q

K investment stradegy

A

Investment optimized for care and or development of offspring
- Produce fewer offspring BUT hope all surive –> add more resources to make sure they do

Example – elephants

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150
Q

Example K stradegy

A

Elephants – If they all survived to reproduction – in 44 generations they whole earth would be elephants
- Means that even for the slowest growing organisms postulate #3 needs to be true (still need to have variation in survival + reproduction)

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151
Q

Most important postulate

A

postulate #4 – survivorship + reproductive vary as a function of traits

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152
Q

What do we mean in Postulate #4 – surovorship + reproduction vary as a function of traits

A

Means that variation in survival is mathamatically connected to varaition in traits
- Survive and reproduce as a function of varying traits
- means that rates of mortality and reproductive sucess are NOT uniformly distributed across the population in regard to certain phenotypes
- Means that individuals with a certain phenotyoe value are more likley to survive + reproduce

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153
Q

Example of uniformlity distributed

A

In the image – the trait is not affecting survival –> there is no diffrence in suvivorship between individuals with trait or without the trait
- In this case natural selection is not active
- Have uniform distribution

Uniform Distrubution = no correlation = failes the 4th postulate

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154
Q

Uniform distribution

A

probability of y does not vary as a function of x - everyone in the population has the same chance of surviving and reproducing, regardless of phenotype

***Means that natural selection is NOT active – fails 4th postulate

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155
Q

Not uniform Distribution

A

Image = not uniform distirbution – one trait value (individuals with certain traits is NOT surviving) BUT trait values in the center (individuals with different traits) are surviving

***have a difference between survivorship –> means that what trait you have matters for survival
- there is a relationship between trait and survival
- Trait = affects probability of survival
- here posulate #4 is true

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156
Q

Example where postulate #4 is true

A

Coat color in mice –> whether mice survive is based on coat color

In dark soil = dark coast allows you to camaflouge better = survive better

In light soil = want light coat

***There is a connection between coat color and liklihood of surviving

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157
Q

Example of Natural Selection

A

Gulls – In a field of Golden Rods
NOTE: many insects = specialists for golden rods –> Many inescts make a Gull on the Golden Rods
***Goldren Riods = well studied in evolutionary studies

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158
Q

Insects Making Gull

A

Gull = purely plant tissue

Insects induce it in the plant –> then insects lay egg in the plant and the plant secretes hormones to trick the plant to make a structure that benefits the insects

 - The Vascular tissue = adds defensive compunds around the Gull 
 - Making the Gull is ONLY costly to the plant --> the plant is really making a house for parasite 
- Affects plant replication 
- Gull = puts fitness cost on plant 
 - Gull = hujacks the plants genome
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159
Q

Example – What shapes the evolution of Gall size

A

Look at 4 postulates:
1 – Is the Gall size variable –> YES

2 – Is the Gall size heritable –> YES
- Hard to test

3 – Do all flies continue to the next generation – is there variability in survivorship – YES

4 – Is fly survival and reproduction uniformly distributed – YES
- Look at natural history

***All 4 postulates are true = makes a relationship between probability of survival and size of gall = selection is occuring

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160
Q

Testing if gall size is hertibles

A

Grow clones (meaning that they have the same genotype) in greenhouse and look at parent vs. offspring

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161
Q

How do you know that all flies continue to the next generation

A

In 3 generations = it would be over 15 million flies if there was no diffreence in survivorship AND we know that most flies don’t move more than 25 meteres – since we do not have 15 million flies in 25 meters = know there there is differntial survival + reprduction

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162
Q

Seeing fly survival and reproduction is uniformly distributed

A

Look at Natural history + look at Gall size

***record gall size and open them up to record the fate of the fly larvea (look at gall size vs. survival)

Need to look at the parasotic insects that attck Gall flies
1. Beetle – most get attacked by beetle –> WITH beetles there is some varaition in survival BUT mostly the same atttacj rate no matter the Gall size –> Means that the attack rate IS uniformly distributed = there is no difference in survival because of Gall size = means natural sleection is NOT occur
- here survival rate is the same for all gall sizes

  1. Wasp species –> The probability of getting attacked by a wasp increase as gall size decreases
    • at 25 nm you are almost immune to wasp –> Here there is a relationship between the trait and suvivorship = means that natural selection is occuring
    • Not uniformly distrubuted = having the trait affects your survivorship = NS is occruing
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163
Q

Why doesn’t Gall size just continue to increase – why are they not all Huge Galles

Why is there NOT runaway selection

A
  1. Wasps are NOT the only source of mortality

Example – birds also each the galls (birds eat the insects in them)
- Birds go after the bigger galls (bigger galls have lower survival)
MEANS that there is selection in both directions –> the intermediate size is the best

Result: Get stabilization state – NOT getting runaway selection because NS is not just optimizing one thing at a time

  1. There is a difference acorss popultions + difference across years – NS process = go back and forth all of the time
    • Looking at different locations and within the same feild in different years the gall sizes change and they change in different conditions –> NS regimes are NOT fixed through time – forces imposing NS change so have long term dynmanic shift
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164
Q

Runaway selection

A

When the traits just most so far from to be the most fit (Ex. Gall size just ciontniuing to increase to be HUGE galls)

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165
Q

Stabilizing Selection

A

Individuals with the intermediate trait values have the highest fitness –> When teh intermediate trait is favored
- Sleection won’t go in one direction forver because the end point is not the best – the best is something in the middle

Ex. Gall size – because bigger is good for bird protection but small is good for wasp protection = the intermediate size is the best

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166
Q

Physical Fitness + Darwinian Fitness

A

They can be related BUT they might not be

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167
Q

Fitness in Vernacular

A

Conjured a lot of meanings – Strength + Stamina + Speed

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168
Q

Darwinian Fitness

A

The extent to which an individual contributes to future generations
- Not neccesarily what we think of as “fitness”

***amount of individual you contribute to the subsequent generation

***Need to think of it in terms of LIFETIME reproductive output

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169
Q

Survival + Fitness

A

We often think of “survival of the fitest” BUT survival is not enough

***Survival is a neccessary compoennet of fitness BUT it is not enough for fitness

Survival = only ONE part of it –> Need to survive to the point of reproduction – survival is needed for fitness BUT also need reprouctive component (need repriductive sucess)

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170
Q

What is needed for fitness

A
  1. Survival
  2. Reproduction

NEED – survival + reproductive success

Firness = Survival –> Reproduction

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171
Q

Post reproduction survival in Fitness

A

AFTER reproduction – can still survive after reprpduction –> That survival might not have to do with fitness because you already reproduced the amount you will in your lifetime

***Shows that survival is NOT the only part of fitness – some types of survival might not even be part of fitness such as survival after reproduction

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172
Q

Components of Fitness

A

We can define many compennets of fitness (BUT they are organism soecific)

Example for sexual organism:
Surival –> Mating success –> Fecundity
- Need to survive to the point of reproduction

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173
Q

Fecundity

A

Number of offspring you produce + can include parenting sucess
- Includes parenting sucess IF offspring learn traits because then you arte keeping them alive
- This is NOT inclduing genes of offspring traits

***Part of mom’s fitness = how well she can protect her kids BUT her genes are not part of the kids fitness

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174
Q

Mating Sucess

A

Looking at traits that might contribute to mating sucess

Example – competition with males + locating a mate + co-population + fertlization
- You might have a moose that is good at getting a mate but his sperm doesnt work making his fitness zero

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175
Q

Is offspring survival part if fitness of parents

A

Depends of the traits in question – need to think about whose fitness it is
- Part of mom’s fitness = how well she can portect her kids (that is mom fitness) BUT part of kids fitness is based on the genes from mom

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176
Q

Fitness in life histories with multiple mating events

A

Need to think of it in terms of LIFETIME reproductive output

Have survival –> Mating success –> Fecundity –> GOES BACK to survival

KEY for seeing if trait affects fitness = does it affect lifetime reproductive sucess

***Fitness = might not only have a single round of reproduction – if life historiues with multiple mating events

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177
Q

Key for seeing if trait affects fitness

A

Does it affect lifetime reproductive success

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178
Q

Example Orthology

A

Duplication evnet in PMP22 gene – makes sense as homologs that arose in common ancvetro of human + chimp + baboes after split wioth gprilla
- Shared because of homlogy –> tells us about biological reality of relationships of organisms

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179
Q

Molecular homology

A
  1. Junk DNA
  2. Look at functional things that are homologous –> look at biochemical pathways
    • Often have homologous biochemical pathways –> same genes for enzymatic function because of homologty
      -Same mechanisms + pathways because inherited from a common ancestor
      Example – Aquition of mitocondria
    • Many biochemical underpinning s of life were laid down a very very lomg time ago

Molecular homology = extent way beyond closley relate mamales

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180
Q

Why is Junk DNA good evidence for homology?

A

Good evicence because can’t be convergent evolution

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181
Q

Aquisistion of mitocondria

A

Example of molecular homology – occured because MRCA of all extant Eukaryotic organisms
- Homologous across ALL Eukaryotic
- Critical in history of life
- Impirtant molecular homology

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182
Q

Time in evolution – need to contemplate the time involoved

A

To know time = look at time scale for porcess in the world and then scale up

Example – whales (Time from evolutuon)
Mammal –> Whales = took 55 MY
- Huge chnage in physiology + Morphology
- 55 MY = brief in the hirtosy of the earth
- 55 million years vs. history of animal life → small – 10% of animal life as we know it
- Histiory if all animal life vs,. History of the earth → animals = very small part in history of the earth
History if form = very small – took all of the time befire to build all biochemical processes

ALL took tremednous amount of time – change from 1 generation to the next = can be scaled up to the history of life
- Diversity seen in animal life today = looking at huge time scale

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183
Q

Transional fossils misconception

A

People think that transtional fossiles = direct missing link

***They are not missing link they are just a branch between two points – represents a brant that has some chnages but not all
- Branching point shows things that are no longer alive BUT show us the order and where these things occured

Point of TF = that they tell us the order of events –> tell us the order of evolution – show us the order and where these things occured

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184
Q

When can population evolove

A

If the 4 postulates are trie

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185
Q

Exponetial growth Example – Aligator snapping turtle

A

Example of a popultion that people think might be slow growing – shows that they would still become unstable very fast
- Have potential for out of control growth (Expo growth) in population that we think would be slow

Prompt: Each female lays 15 eggs at a time (15 eggs per clutch)
- In the current popultion the ratio of males to females in the offspring is 2:1

Question – if we introduce a male and female turtle into the lake –> how many total (male + female) grandchilren will they have if all of the females survive to reproduce

Reminder = ONLY include females in the equations

We know:
- Yo (starting popultions) = 1 –> because only females are included in teh equation – start with one male and one female BUT only include the ONE female in equation
- T = 2 geneterations – because asking for grandchildren = Parents –> Children –> grandchildren = 2 generations
- X = 5 eggs –> Because we know that its is 15 TOTAl egges per clutch (which includes male and female eggs –> Apply the 2:1 ration = 10:5 males:females = 5 female eggs per clucth (ONLY inlude females in equation)
- yT= ?

Yt = 1 X 5^2 = 25 Females –> X:25 (2:1) –> 50:25 –> 50 + 25 = 75 – Answer: 75 total in 2 generations
- 75 grandturtles come from just one clutch of eggs in each generation

IN REALITY – a female thyat survives to adulthood has an everge lifespan of 70 years
- If a turtle as her first clutch at 12 = she has 58 clutches in her lifetime
MEANS her reprodctive rate = NOW 290 (Because 5 X 58 clutches) –> 290 female eggs in lifetime

THEN Yt = 1 X 290^2 = 84,100 female granturtles
apply 2:1 –> 252,300 total grandturtles
- If they all survived – in just 2 generations = 252,300 – know that this won’t actually happen because everyone surviving almost never happens

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186
Q

How should we think about fitness

A

Need to think about fitness as a whole

To think about fitness (consequnce of individual adding to gene pool) = need to think about survival and reproduction – need to think of BOTH survival AND reproduction

When we’re thinkning about traits and variation we need to ask “what are the conseqeunces of contributing to the gene pool in the next generation”

***Fitness is sometimes counter intuative

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187
Q

Fitness logic

A

Fitness is sometimes counterintuative – the biggest + stringest + fastest + feircest isn’t neccesarily the fittest

Example – Fitness of Gulls
- Can look at it in two ways they can get kills
1. humans shooting the seagulls –> here there are no traits that would protect them
- Whether they get hit = by chance –> there is no heritable traits that are under selections in this context
2. Using Trained raptors – they chase the individual –> maybe there is a trait tat plays a role in whether they get eaten by a falcon
- Can catagorize the dead bird based on muscle density (Have normal + More + less) – most of the indiviudals were normal but had some that were higher and some that were lower

RESULTS:
1. For the shooters – the probability of survival is the same –> therte is a unifrom distrubtion across trait values – survival is not impacted by muscle condition
2. For the falcones – still have the same muscle distribution across popultion BUT now the probability of survival is NOT the same
- poor muscle = less likley to survive (might be less agile + Slower)
- normal msucle = higher survival than the other two
- More musle = likley to get killed –> SHOWS that higher musclar physical fitness here DOES NOT EQUAL biologic fitness (Example of counterintuative to how we think of physical fitness)

Here – intermediate os the best = example of stable selection

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188
Q

Example #2 of counterintuative fitness – Dogs

A

Question – Which of these dogs has the highest fitness

Fitness = depends on the conetxt – can only define fitness in the answerment the organisms is currnetley in

Answer: We can’t know which will repdouce more just by looking at them – the actual condition of the organisms + their ability to interact in the envirnment doesn’t mean anything about reproductive sucess
- Fitness of the Left = zero – bevcause he has no testicles BUT we would not know that inofmration without bieng given it
- Fitness of the right is greater than 1 assuming it can breed

NOTE – need to keep in mind lietime repdouctive sicess

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189
Q

Example #3 of fitness – Dung beetle

A

Dung bettle fitnes can be counter intuative for reprductive sucess among fertile individuals
- The Dung beetle males = build tunnels for females and girad them – while the big heavily armored males are fighting the smaller hornless ones sneak into the tunnel and mate with the females = results in 2 stradegies for reproductive fitness

OVERALL – shows that fitness is NOT straight foward – shows that fitness is complicated and we need to keep that in mind

Here = have 2 forms of fitness:
1. Smaller (no horns) –> bypass the fighting males and sneak in
2. The bigger ones guard and then mate with females

***This helps explain why we still have smaller males – shows slection for one direction and the other

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190
Q

Key points regarding humans

A
  1. Wehn we talk about Darwinian fitness we are NOT making value judgements – we still have to think about lifetime reproductive sucess (and this is not always easy to preduct)
  2. If we make analogies to humans – to get fitness in humans = we just think about reproductive sucess
    • We cannot make value judgements on phenotype –> way we use fitness = hard to seperate from the biologic definition
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191
Q

Misconceptions about evolution

A
  1. individuals evolve – REALITY = selection acts on individuals BUT individuals don’t evolove
  2. Natural sleection can see into the future – it cannot
  3. Selection adds more varaition – REALITY is that selection acts on existing varaition in popultions
  4. Selection results in perfection – NOT TRUE
  5. Selection favors complexity – NOT TRUE
  6. Being evolutionarily advancd – subjective
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192
Q

Level of evolution vs. Level of selection

A

Evolution = population level
- Evolution = allele change from one generation to teh next –> change in allele frequencey in a popultion over time = populatoions evolve

Selection = acts on individual – fitness is based on individual

Selection = acts on individual BUT indoividuals don’t evelopve populations eveleve

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193
Q

Change in individual

A

Change in individual IS NOT evolution – change in an individual is JUST development

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194
Q

Darwin vs. Lamark’s views

A

The crux of the difference between darwin vs. lamarsck was veiws on the mechnaism behind decent with modification
- Lamarck = change in indivual that is passed down

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195
Q

Natural selection looking into the future

A

Natural selection = CAN’T look into the future
- NS = purley mathamatic process within parental generation

Result = evolution lags a generation behind the selective pressures
- NS is bloind to the future – it can only repsind to the conditions in the cirrent generation at the time –> NOT prepparing for the next generation
- NS = only responds to the crrent envibrment – not looking to the future
- ONLY the current conditions affects differnce in repdouction and survival

196
Q

Lag in NS

A

Because NS can’t look in the future = have a lag a generation behind the selective pressure
- The popultion adapts to parents conditions – the offspring might be in different conditions that they might not be well adpated for
- Offspring are adapted for their parents enovrment = have lag
- Evolution is a step behind if the conditions are changing rapidly

Example – Avgerage Gall size changes from year to year – the Gall size is optimal from the past year = have lag
- Size of galls in one generation = based on parent conditions

197
Q

Variation + Selection

A

Selection acts on the existing varaition in a given popultion – IT DOES NOT add new genetic varaition

***Nothing about Natural selection makes varaition – NS is not adding variation BUT that doesn’t mean that novel traits are not evolving

198
Q

How do novel phenotype evolove

A
  1. reshuffling of genetic varaition
  2. NS is in concert with two evolutionary forces (Mutation + Migration) – Get novel varaition through mutation + Migration
199
Q

Example of selection acting on existing varaition –Avergae oil in kernel

A

Start = have 4-6% – Avg = 5%

THEN selected for increased oil content –> Pushed popultion outside of the bounds from the start BUT it moves outside of the bounds ONLY based on exiting variation (pushes outside ONLY because natural selection is reshuffling)

Have 3 genes that influence kernel Oil – all three have allele for 5% phenotype BUT some individuals might have an allele than increase the oil
- The +2% alleles = at low frequencey in the orginal popultion
- Each +2% allele contributes to varaition – likley to have 1 +2 alelle per indivual in the popultion BUT then as NS acts on the popultion you can have more indivudals with the +2% allele – the +2 alleles are bieng elected for – NOW you are increasing the amount of +2 alleles in the popultion – with the increase frequnecey there is a higher change than an indivual gets 2 +2 alells – now you have multiple + 2 alleles = now have increase in oil content
- As NS acts on the popultions –> the indivuals with +2 alelles are selection = increase frequnecey of +2 allele = increase chances of getting + 2 allele

HERE = you are reshuffling the varaition that is already there – you change the allele freqeunecey –> Leads to you pushing outside the bound of the parent population

200
Q

NS + phenotypic bounds

A

NS takes varaition and psuhes the distrubution outside of bouns of parents varaition – outside of phenotypic bounds of distrubution because of reshuffling

***Mutation and migration explains novel phenotypes even more so

201
Q

Selection + Perfection

A

Selection does NOT result in perfection

***Evolution is constrained – evolution can’t optimize all traits simultanously

Example – Galls – Can’t optimize protection from wasps and protection from birds at ones – because they are conflicting traits (one is bigger and one is smaller) = can’t optimize both at once = constrained

202
Q

Selection + Complexity

A

Selection DOES NOT favor coplexity – life has increased in complexity iver time BUT NOT because selection is favoring complexity
- It is intuative that complex orgainsms exist now that didn’t in the past –> potential complexity of animal life – might see this history and assum ethat there is a reason that NS favors complexity

203
Q

Fitness + complexity

A

Fitness can just as easily incluse loss of complexity as it gain include gain in complexity

***People think that becoming less complex = de-evolution –> It is not de-evolution – just regular evolution (fitness in these cases is just getting rid of complexity)

204
Q

Lamarck + Complexity

A

Part of Malarcks ideas was thinking that a driving force was to increase complexity over time

205
Q

Exmples of Loss of complexity

A
  1. Flightless birds – came from flighted bird (flight = more complicated = means that things decrease in complexity)
  2. Organosms living in caves = lose eyesight
  3. Many insects = live sessile life
  4. Parasitc organisms = lose complexity (some thing that ere are more parasitic organsims than any other = means that this loss in complexity happens a lot)
206
Q

If Natural Selection doesn’y favor complexity –> How did we increase in complexity

A

Example – Drunkard’s walk – if a drunk person stumbles out of a bar and he doesn’t know where he is going
- he is walking from the wall –> Gutter

HERE – it is inevutable that he will end up at the wall
- Since he can’t go back past the wall = he will eventually end up in the street – because there is a limit in one directed imposed by the wall = he needs to end up on the street

SAME THING = happens with complexity over time
- In evolution we have a limit “Gould’s left wall of biocompleicty” – we have evoloved in a compltley random way (we go back and forth in both directions) BUT we can’t go past the wall
- IF the wall wasn’t there = then the space of complexity would spread to both sides (because less and more complex would happen) – since it is going in both directions in this case the average complexity would stay the same BUt the variability will change
- BUT with the wall = can’t go past a certain point in one direction = vraiabluty can increase (can go in one direction) BUT can’t go in the other = the average complexity CAN ONLY increase because there is a limit on one side that we can’t go past

***In this way a directionless process leads to big increase in complextity iver time – inevitable paty of process

207
Q

Increase in complexity process

A

Increasing complexity arises from a passive undirected process
- NS process is NOT in the direction of complexity (it is a directionless process) YET we have an increase in complexity
- We evoloved in a completley random way – go back and forth in both directions BUT we can’t gp past the “wall”

***In this way a directionless process leads to big increase in complextity iver time – inevitable part of process

**Get overall increase in complexity BUT without Natural selection actually favoring complexity because natural selection does not favor complexity
**
Still get pattern of increase in complexity in directionless process

208
Q

Drunkards wall in evolution

A

In evolution = have a limit (similar to wall in drunkard’s example) – the wall = Gould’s “left wall of biocomplexity”
- This wall = limit to lack of complexity that we can have – it is the least complex thing that can still be alive –> we can’t go past it

209
Q

Being Evolutionaryly advanced

A

VERY subjective – humans think that they are the most advanced BUT that is completley subjective
- Humans have not evoloved more than any other organisms –> all orgainsm today have been evoliving for the same amount of time

Example – Humans vs. Platapus
- Humans = evloved live birth + mamamary glands after they split from platapus – since this evolution is more recent = seems more adavanced BUT that is just our perspective
- Platapus – evoloved their own traits ince the split (venom + electroreception – they can feel the nerves of other fish) –> from the perspective of the platapus they are more advanced

210
Q

What prevenyed Universal accpetance of NS for decade?

A

Some gaps in knowldge
1. The nature of novel varaition (people didn’t know where novel varaition comes from)
2. The natire of inheritance
- Many of the critisms were reasonable given the level of understanidng – critisms makes sense based on what people knew

***Issue = was acceptance of the mechanism of change – NS wasn’t beleived

211
Q

Understanding the nature of varaition

A

Peolpe did not know this = didn’t beleive NS
- Commanality of mutation was not appreacted until genetic work with Drosphilla in 1900s STILL the natire of mutations importance for evolution was questioned for decades

212
Q

Question about mutation in evolution

A

Is it one rare mutation or is it a build up of many small minor ones (Gradual vs.. Saltation

NOW = we know that saltation is not how it works most of the time – we know it is usally small changes over time

213
Q

Saltation

A

Jumping – Idea that there is a mutation that just reframes whole organism and then acts quickly on it
- People thought IF this is the way it works then mutations would cerate monsters
- Question = was evolution dirven by catastrophic mutations that lead to “hopeful monsters”

214
Q

Nature of inheritance understanding during darwin

A

Mendle was active around the time The origin of species was published BUT his work remained obscure for decades – Mendles work wasn’t published at the time and was not rediscvievred until the end of the 19th century –> people didn’t now how inhertanve worked + the ideas at the time didn’t work well with how natural selection works

IN the meantime popular ideas about inheritance didn’t work well with Darwinian selection

215
Q

Idea of Inheritance during darwins time

A

Blending inheritance –> people thought that some asoect gets passed on and there is some blending that mix to make offspring
- People know that offspring look like parents BUT thought it was a blend of traits

***Blending = doesn’t work well for evolution by NS
- Blending = not a mode of inheritance that allows evolution to persist

Example – Start with an all blue population → THEN have a spontaneous mutation that makes a red color → Say the red is favored → if blending of traits is true the offspring would have a mix of red and blue = would get purple offspring – some might say purple and some might mix more with blue = goes back towards blue
- In this case the intial red gets dilluted over time (NOW you have a dilluted version of the mutations and never get the red again)

***In blending you never get the instial red again – the effect of the mutation doesn’t matter because it is always diluted through time
- If this was true NS wouldn’t work

216
Q

What was the mechansim of evolution missing

A

The mechanism of evolution was missing a mode of inheritance

217
Q

Issue with blending inheritance

A

It does not work well with evolution by natural selection – because over time you only get a dilluted version of the mutation (never get the original mutation again)
- Keep losing the phenotype – new variation goes away
- Varaition goes away

218
Q

Debate about traits after mendle’s work

A

Discrete vs. Continous traits – if we have discrete genes how can we see continous traits (Such as height + cold tolerance)

Question: How do we reconcile the discrete in Mednle’s work with continous traits

219
Q

Debate of Discrete vs. continous triats

A

Had two camps:
1. The Mendials
2. The Biomatricians – measured things and found that very few things lined up with mednles work (they found that there were very few discerete traits + couldn’t see significant Mednelian genetcics)

Question: How do we reconcile the discrete in Mednle’s work with continous traits

220
Q

Continous trait

A

Can be any value – not discrete trait

Ex. Cold tolerance + height

221
Q

Issue in Mednle’s experiments

A

HE got lucky – the traits that he happened to work with just happened to be discrete traits (they were all or none traits)
- He only looked at discrete traits
- Part of the reason it took people a while to know how heretibility worked is that continous traits often include many genes –> when people found Mendel’s work and looked at some organisms there were some traits that worked BUT there were some that were more complex in nature such as continous traits – so they did not know how heretibility if its not as simple as Mendle’s

***It took deciades of people arguing to understand to connect complex phenotypic varaition and heredity

OVERALL – people had issues with Mendle’s work because his work failed to epxlain the heredity in continous traits

222
Q

Quanatative genetic

A

The study of Heretability of complex traits

223
Q

Modern Synthesis

A

The reconcilliation between the Mendelian and Biometric ways of thinking with Darwinian Evolution

IF people know Natural selection based on phenotypes VS. people know how heretibility works – THEY needed a way to bridge the two

Modern Synthesis = shifted towards genetic understanding of evolution and biologic varaition

***led to paradigm shift

224
Q

Point of Modern Synthesis

A

Shift towards a genetic understandng of evolution and biologic variation
- Modern Synthesis = need to think of evolution as genetics and allele frequency

***reframed evolution explictiley around popultion

***The new persective allowed us to refarme the postulates of Natural selection

225
Q

Importance of recolciloing mendelains and biometricians

A

There was this impediment to understanding eveolution because of the debate – reconciling the camps allwoed us to have an undertsanding that modern biology uses today

***Reconciliation = occured because of modern synthesis

226
Q

What did modern synthesis look at

A

studies natural selection as mechanism and other mechanisms of evolution – understanding change over time

227
Q

Understanding of genetics during modern synthesis

A

During the time there was a framework of understanding basic genetics – now scaling up the basic genetics of the family level – allowed us to understand the mechansim of change

228
Q

MS in my own works

A

Basically there was this debate where they had continous traits and Mendle’s finsings couldn’t epxlain the heretibability behind them – this was an impediment in understanding natural selection as the mechansim for evolution

***This debate was reconciled by the modern synthesis

AFTER the reconcilation they wwere able to turn the phenotypic undertsanding of evolutrion and synthesisze that with waht we know about how heretibility works

The synthesis then reframed evolution to be on popultoon level + scaled up our undertanding of geentics to popultoion lavele –> ON the popultion level we can now understyand mechnaism of change and using that new understanding we reframed the postulates of natural seleection.
- NOW have genetiocs worked into Evolution by NS

***Modern synthesis = explains evolution as a fundementally genetic process

229
Q

Outcome of Modern Synthesis

A

Restated the four postulatesin explicitly gebetic terms

MODERN synthesis = explains evoluton as a fundementally genetic process

***The postulates are the same conceptutally but are tweaked to be about genetic varaitions

230
Q

Postulate #1 After Modern Synthesis

A

Varaition among individuals results from mutations creating new alleles arsing and segregating in populations
- Varaition had to do with varaition in alleles

BEFORE – was about phenotyouc variation – now making it about genetic varaition

231
Q

Postulate #2 After Modern Synthesis

A

The inheritance is the result of allelic variation passing from parents to offspring
- Traits are heretible

BEFORE – phenotypic varaition – NOW allele varaition – connects parents phenotypc to offspring phenotypes

***Connects offspring phenotypes to parents phenotypes

232
Q

Postulate #3 After Modern Synthesis

A

Through differential survival or reproductive sucess not all individuals contibute the same amount to the following generation
- Really just the same thing (nothing is different)

233
Q

Postulate #4 After Modern Synthesis

A

The probability of contributing to the next generation varies as a function of an individuals genotypes
- Alleles at a locus affect if you survive and reproduce
- Shows genetic version of Natural selection

BEFORE – stating the relationship between phenotype and S/R BUT now S/R are difefrent based on genotype

234
Q

Charts before and after Modern synthesis

A

Before = looking at charts that compared phenotype to the probability of survival AFTER looknig at charges that look at genotype and probability of survival

BECAUSE phenotype is based on genotype = can compare the proabbility of suvival between genotypes (because the diffreent genotypes is what leads to the phenotypes that allow some to survive more)

235
Q

Quanative genetics

A

Understanding the connection between selection and variarion on alleles to phenotypic distribution
- Looking at how envirnment affects variation + how Heredity occurs + How the genotypic distrubution responds to Natural selection

***Understanding the connection between discrete inheritance and continous traits

236
Q

Why is it important to talk about genetics in evolution

A

Because evolution is the change in allele frequncies in popultion through time = need to establish the rules by which alleles are passed between generations

We are building a null model –> rule of inheritance between phenotype are used to make null models in popultion genetics

237
Q

Making null models in popultion genetics

A

Make null models using the rules of inheritance between phenotypes

238
Q

Gene

A

The discrete functinonal unit of heredity – refers to any variable geentic locus
- Parent –> Offspirng – is NOT diluted

***What sticks around in generation of offspring

239
Q

Gene in other context vs. gene in this class

A

In other contexts – gene often refers to a segment of DNA that contains a transcribed region andnits regulatry regions

This class – think of gene as more than just protein coding region
- We think of it more broadly because there are parts of the genome that affects phenotypes = affects heredity + we are still intersted in variation that doesn’t lead to phenotypes
- In evolutioon – we are intersted in heretible varaition more broadly that jist protein regions

240
Q

Locus

A

Specific location in the genome

241
Q

Genome

A

Total herediatry information in an organism

242
Q

Genotype

A

The specific allelic composition of an individual at one or more loci

Variant at a locus – doesn’t need to be a protein coding gene

243
Q

Gene duplication evens

A

Have one locus that duplicates and inserts somewhere else in the genome

244
Q

Example – Say we have a gene duplication event mutation where a locus sequnce gets copied to another location (identical sequnces) – Is this two genes or 1 gene?

A

ANSWER: 2 genes – because it is 2 loci (gene = any variable genetic locus)
- It can be the exact same protein but since it is two loci = it is two genes

***Because they are two loci = they are inherited seperatley (can be passed down irrespective of each other) = 2 genes

245
Q

Alleles

A

Variant forms of a genetic locus

Example – can have. aC instead of a T OR can have an Indel OR can be varaint bases near each other than are inherited together

***Different alles could affect phenotype BUT can have two alles that still make teh same phenotype (diffreent sequnce but still leads to same phenotype)

IMAGE – thigs on the side = shows the phenotype for each locus

246
Q

Polymorphism

A

When there are multiple variants

247
Q

Gamete

A

Specialized haploid cells resulting from meiosis (in sexually reproducing taxa)

248
Q

Meiosis (overall)

A

Diploid –> Haploid (makes sperm/egg)

249
Q

Calculating how many possible gametes can be produced

A

2^n – n = number of pairs of heterozygous chromosomes OR number of heteozygous loci

***Based on the genotypes across homologous chromsomes = can look at all of the possible gametes produces

Example – 2 alleles at 2 loci = 2^2 = 4 gametes

250
Q

Why are Mednle’es “Laws” and not Laws

A

Because his “laws” are NOT absolutley strict – they are good most of the time but they are not asbolute

251
Q

Mendle’s “Laws”

A
  1. Law of Segregation
  2. Law of independent assortment
252
Q

Law of segregation

A

Homologous chromsomes seperate during meiorsis so that ONLY one copy of each gene (one allele per locus) occurs in each gamete
- If the parents are diploid )have 2 copies of each locus) –> only one copy ends up in gametes
- Each gamete carries one copy into the gamete pool to form zygotes

***This is the closest one to a law – because it works most of the time

253
Q

When does Law of Segregation Breakdown

A
  1. Non-disjuction events + Mitotic errors
    • Can get 2 copies OR no copies

Example – trisomy 21

  1. Chromosomal fissions –> large scale chromosomal events
254
Q

Law of independent assortment

A

Allelic varaition at different loci are passed to offspring independently
- The probability of getting one allele at one loci is independent from the probability of getting a different allele at a another loci (alleles at different loci are inherited independently of each other)
- Alleles of difefrent genes are inherited independently of each other

***ALL multi loci gametes possibilities are equally likley
- The probabilities of alleles at different loci being inherited are indepent of each other

***leads to a mix of mom and dad alleles in gametes (because might get mom at one loci but dad at a different loci)

255
Q

When is the law of independent assortment true?

A

True when the loci are on different chromosomes + If the loci are far apart on the same chromosome

256
Q

Recombination

A

Swapping of alleles between homologous chromosomes – Likley to happen a few times on each chromosome during meiosis

END – a new version (with a mix of maternal and paternal alleles) ends in gamete

257
Q

How to know if two loci are indepent

A

They are independent if the likleyhood of a gamete with both loci is 25%

BECAUSE if they are indepent then can multiply probability

P(one allle at loci 1) = 0.5 (If have 1 M and 1 P = Probability of Either M or P is 1/2)
P(one allle at loci 2) = 0.5 (If have 1 M and 1 P = Probability of Either M or P is 1/2)

P(one allle at loci 1) X P(one allle at loci 2) = 0.25

***If they are independent then the chance of getting both is 0.25

IF the frequency is NOT 0.25 then ther are NOT indepent (iof the freqincey is 1 or 0 then they are completley dependent)

258
Q

Linkage

A

Deviation from expectation that two alleles are indepent of each other

***If the chance of getting 2 alleles is not 0.25 then they are NOT indepent = they are linked in some way

259
Q

When does Independent assortment occur

A
  1. During metaphase
  2. During recombination
260
Q

Recombination + Indepentdent assortment

A

IF you have recombination then you are equally likley to get ALL combinations of alleles (MEANS that alleles at different loci are indepent of each other) BUT if recomnbination is not equally likley then you change the probability of getting combinations of alleles = Lose independent assortmement

261
Q

Deviations from Independent Assortment

A
  1. Linkage
262
Q

Deviations from Independent Assortment

A
  1. Linkage
263
Q

Linkage

A

Unlikley for cross over to happen when close together = NOW has some alleles occuring together more than others
- Have a non-random distribution of multi-loci genomes (Not 0.25 for all)

Example More AB than ab or Ab = Means that A and B are no longer inherited indepentley of each other

***Often due to a physical linkage – close proximity of the same chromsomes BUT not always

264
Q

Recombination

A

Event in meiosis that generations haploid multi-locus genotypes that differ from the parents
- get genotype that neither oarent has

265
Q

What is included in Independent Assortmant

A
  1. Recombination (within chromsomes)
  2. Lining up of chromsomes on metaphase plate (Assortment of chromosomes)
    • Always have this
266
Q

Importance of recombination

A

Important part of independent assortment – anything that limits recombinations = causes devaitions from mendle’s laws

267
Q

Do you always have Independent assortment between different chrosmomes

A

YES

268
Q

Do you always have independent assortment within chromosmes

A

NO – might have linakge = no recombination = no IA (THIS IS A TIME WHERE MEDNLES LAW BRAKS DOWN)

269
Q

Linkage

A

Any breakdown of independent assortment

MEANS that allels at different loci are inherted together more than exopected by chance – alleles at different loci are not being inherited independently of each other

EXAMPLE – if AB is more likley than ab (means that A and B are no longer inherited independently of each other)

270
Q

Modifier models

A

We can change models to account for linkage

270
Q

Modifier models

A

We can change models to account for linkage

271
Q

Probability and Law if independent assortment

A

Because the probability of inheriting alleles at different loci are indepent = can multiply the probability of getting the allels

Ex. P(red allele at locus 2 on chromosome 1) = 0.5
P(organe allele on chrosmome 2) = 0.5

Probability of getting Red AND organe = 0.25

***Because they are inherited independently of each other = can multiply them together

272
Q

What will proabbility be is IA is true?

A

The proabbility of all possible gametes will be in equal propertions

273
Q

Punnent Squares (Overall)

A

Visual representations of the probabilityes of getting a specific gamete – visual representation of probability of genetic varaition from 2 individuals
- Shows Mendle’s Laws

***Stems from mendles first two laws

274
Q

What do punnet squares show

A
  1. Show Mendle’s Laws
  2. Show varaition in gametes – shows the types of offspring and the frequencey at which they occur
275
Q

Punnet Square for single locus

A

***Can look at the frequency at which genotypes occur

276
Q

Punnet Square for Two loci

A

Can see that there are 4 haploid gametes per individuals THEN look at how each indiviudlas gametes combine to pass to zygotes

***Can see genotype and phenotype frequncey

TWO LOCI genotype ration – 9:3:3:1

277
Q

Genotype Frequcney in Dihybrid cross

A

We are able to determine the frequncey of genotypes in the next generation from the gamete pool of the mating pair
- Can see the probability of producing 2 phenotypes

278
Q

What is the result of Punnet square

A

You can see the frequencey of genotypes in the next generation form the gamete pool of the mating pair
- Can se the gamete pool in the cross (result of the cross is the gamete pool)
- can see the probability of producing certain phenotypes

279
Q

Gamete pool

A

The set of all copies of all gamete genotypes in a populations that could potentially contribute to subsequent generations
***Is the inside of the punnet square

280
Q

What is the punnet square

A

A representation of the probabilities of zygote formation across gamete pool

281
Q

Calculating probability of zygote with particular genotypes – what is the probability of forming a zygote with aabb

A

Option 1 – Look at square –> Can see 1/16

Option 2 – There is only ONE way that aabb forms (if sperm has ab and egg has ab)

P(ab sperm) = 0.25
- becasue have 4 possible sperm and all of them are equally likley
P(ab egg) = 0.25
- because have 4 possible egg and all of them are equally likley

P(aabb) + 0.25 X 0.25 = 0.0625 = 1/16

***Since P(ab sperm) is independent from P(ab egg) = the probability of both of them happening is the product of their independent probabilities

282
Q

Example – what is the probability of Aabb Zygote

A

Since producing Aabb with ab Sperm and Ab egg is Mutauklay exlusive from produving Aabb with Ab sperm and ab egg = can add their probabilities together (CAN ADD for ME)
- We wait the probaility that either one OR the other will happen → MEANS that teh combinaed exclusive events are additive

283
Q

AND vs. OR in probabilities

A

AND = X
OR = +

Independent statement (AND statement) = multiply
Exclusive statement (OR statements) = add

284
Q

Expanding mindset of mednialn genetics

A

We can take the mindet of probabilitu events in gamete pool and use it to build a model of mendelian genetics at the population level

285
Q

Complication to mendelian genetics

A
  1. Dominance
  2. Epistasis
286
Q

Dominance

A

The phenotypic affects of one allele masks the phenotyopic affect of another allele at the same locus
- Interferance between 2 alleles at the same locus
- Effect from interaction of many alleles at once locus
- One allele interacts with the other allele that affects phenotype
***It is a type of interaction between allelic varaition at a locus (one allele is masking another) BUT really are habing an interaction between two alleles

287
Q

Issue with dominance (why it is a complication)

A

Is a complication – because it blocks the contribution of one of the parents = interferes with heritability across generation (complicatioes the observation of the correlation between parent phenotyope and offspring phenotype)

***Breaks down the straightfoward relationship between the phenotype of the p[arent and the phenotye of the offspring

288
Q

Misconception with inheritance

A

We need to stop thinkning that inheritance is compltley dominent or completely recessive – there can be different degrees of dominence and recessive
- Not everything is just domient and one is recessive
- Many alleles have intermeduate levels of affects
- Dominence itsself can take different forms

289
Q

Example of dominance – eye color

A

1 Copy of A = stops all phenotypic affects of a

***We know A is dominent to a because the heterozygous Aa look like the homozygous AA

290
Q

How does dominence happen?

A

Depends on the molecular affects of the alleles

Tow ways that dominance is generated:
1. Haploinsuffciencey – dosage affect
- 1 copy of something is not enough to do snoething – need expression of both copies to gave a phenotype
- If only have one copy of allele expressed then not passing the threshold to see the phenotype

Example – might need enough of an enzyme to get over the activation energy

  1. Dominance negitive affect – protein interactions (based on what proteins can interact to form dimers or multimers)
291
Q

How should we thoink about traits

A

Traits should be thought about as being determined by the whole genotype rather than just the presence of one allele

292
Q

Looking at genotypes + fitness

A

You can think of the affects of genotypes with fitness as the phenotype
- can see the relationship of fitness and alleles (can think of fitness as just another phenotype)

Example – is the fitness of the heterozygote like the fitness of the AA or aa
- Can also be incompltelet dominent where Aa is in the middle of aa and AA (this is what is happening most of the time

293
Q

Can teh recessive allee increase fitness

A

YES – fitness affects of a mutation can be purley recesisve

(fitness of aa can be higher than Aa and AA)

In the chart – AA is still dominant because Aa is like AA and not aa

294
Q

Aa as incompletley dominant

A

Here have incomplete dominenace – likely in between

***Assume that this is happening most of the time

295
Q

Fuel for evolutionary forces

A

Variation

296
Q

How do we get information about dominance vs. recessive

A

Natural History

297
Q

Dominanece vs. Epistasis

A

Dominance = interaction within one locus

Epistasis = interaction between different loci

298
Q

Epistasis

A

An effect of the interaction among multiple loci on a phenotype (or fitness) such that the joint affects differ from the sum of the loci completley

 - Means that you can't just add up all of the alleles and know the phenotype
 - Interaction among alleles at different loci 
  - More than one gene affecting a trait 

***Can’t predict the effects of the genotype at one locus without knowing the genotype at another locus (If the answer for the phenotype is IT DEPENDS = know its epistasis)

***Common in nature

299
Q

Epistasis + Evolution

A

Epistasis is a constraint on evolution

300
Q

Complication of Epistasis on inheritance

A

Affects the straightfoward parent phenotype to offspring phenotype relationship

301
Q

Type of interaction in Epistasis

A

Statistical interaction

302
Q

Statistical interaction example – Plant experiment

A

IF looking at plant growth – you are tesing the effect of temerature and of fertailizer Nitrogen level (Looking at low vs. high temp AND looking at Low N vs. High N)

If the results = graph with two parrael lines = there is no interaction and there is an additive effect

If the results = graoh with intersectiong lines then there is an interaction and there is NO additive effect

303
Q

No Interaction Result

A

Have two parallel lines (the slope of the lines are the same) = no interactions + have an additive affect
- Means that the affect of one things (N fertlizer) is independnt of the increase of the other things (The affect of the N is indepent of the increase in temperature)

In Example:
No matter the temperture this is alwats an increase in height when there is an increase in temperature
- No matter what temperture the N will always increase the height and no matter what N level the temperature will increase the height

ALSO the temperature increases the height no matter the NItrogen level

MEANS – that there is an additive affect and they ARE indepent
- The effect of temperture does not affect the affect of Nitrogen
- As the temperture incerases plant height increases AND as N increases plant height increases BUT at either tempertures the plant height will incerases because of teh increases in N and at either N the plant height will increase because of temperture (Means that the affect of N is not dependnet on the N level = means they are indepentdent)

304
Q

When is no interaction not additive

A

If they have the same slope but they are flat

305
Q

Result when you have an interaction

A

NO parralele (the slopes are different) = not additive

306
Q

Result when you have an interaction

A

NO parralele – they intersect (the slopes are different) = not additive
- Since the slops are different there is an interaction

Example –
you can’t predict the efefct of one. ofthe variuables without knwoing the state. ofteh other (The effect of teh temperature depends on the state of teh N – The temperature oncerase plant height but ONLY in high N condition)
- At high N the higher temperture decreases height
But at low N the higher temperature increases height

HERE = need to specify teh state of nitrogen – if you asked how does tempertaure affect plant growth - you would need to say IT DEPENDS – because the way that temperaure affects plant groiwth depends on teh state of N

Since you say IT DEPENDS = you know you have an interaction (because the state. ofone affects teh other)
- Effect of Temperature depends on teh state of N

307
Q

How do you know you have an interaction

A

On a graph – if the slopes are different = the lines interact

On a question – If the answer contains “It depends”

308
Q

Statistical interactions

A

When you can’t predict one varaible without knowing the state of another

Example – can’t know the effect of temperature without knowing the state of N

309
Q

Example of No epistasis

A

Scenrio: Have 3 Loci controlling plant height with 2 alleles for each loci

HERE = if the alles have indepent affect (have no interaction) then you would know the genotype by adding up the effect of each genotype for each allele to get the plant height

Example – A1A1B1B1C1C1 → +1 + +1 + +4 + +4 + +6 + +6 = 22

IF have NO epistasis = they are all indepent –> Then they have an additive affect (each alelle contributes seperatley to the overall height of the plant based on the genotype)
Can know the height of the plant by just adding all fo the effects of each genotype

310
Q

How to know if there is no epistasis

A

Know there is no epistasis if there is no interaction – know if all of the alleles for the locus are additive to give the phenotype

Example – if the plant height is just the sum of the allels for each locus
- We can on there is no interaction of we can predict plant height by just counting the number of the allele for each genotype and adding the individual effect

311
Q

No epistasis

A

There is an additive eefct + there is no interactions – the controbution of each allele is indepent of teh other genotypes
- Indepent contribution of effects of alelle

AABBCC – AA is indepentdent from BB and CC
- A will add an amount no matter the genotype of B (A1 will add + 1 NO matter what the genotype is at B – will add +1 if have B1 or have B2)

312
Q

Changing genotype when have no epistasis

A

If you have a plant. andknow the genotype and then chnage the chantype we will know the different in height between the two genotypes IF there is no epistasis

Example
- We know that the height different between the 2 is 5 inches because we know that the effects of each genotype is additive and. sowe know the height of teh first will be. 22and the second will be 27

***SINCE THERE IS THIS ADDITIVE AFFECT AMONG LOCI = WE KNOW THAT THERE IS NO EPISTASIS

313
Q

Example WITH epistasis

A

In plant example – if we added a new locus D that is part of the hormone pathways
- Locus D does not add height it just affects the hormone production
- IF hace D = have no height in plant

NOW – when you change D to D- you have no stem at all and have no height (have no elongation – stop ability for the plant to grow upwards –> means that since that since the plant is not growing upwards at all so the efefcts. ofthe other allleles. donot matter (no matter what the other alleles are there will be no height – whther is A1 or A2 it would be the same height because there woudl be no height)

MEANS – the other Loci now depend on the state of D (Now if you asked a question of how the height would change if we swicth B1 to B2 you could have to say IT DEPENDS – because now it depends on the state of D)
- Since IT DEPEDSN = means that ther us an interaction = means that there is epistasis

314
Q

Question to know if there is epistasis

A

Question = can you predct the affect. ofan allele based ONLY on that allele itself

IF the effect of the allele depends on the state of another of another allele = then you have episatsis
- If “it depends” = means that there is an interactuon = you have epistasius

315
Q

Plant heigh exmaple of epistasis

A

ONce add in D = we can’t prediect the effect of the other alleles without knwoing the stats of D
- If D+ then they will hadd height BUT if D- then they will not change teh height because there will be no height (Since it depends = have epsistasis)

INteraction = epistasis

316
Q

Sources of variation in a population

A
  1. Genetic
  2. Environmental
317
Q

Phenotype

A

The measurable properties of an organism manifested throughout its life
- Any trait that you can measure

Includes: Morphologocal + Phsyicological + biochemical + behavioral

318
Q

What is contained in a phenotype

A

The phenotype contains everything but usually we just kook at a subset of that
- Includes the TOTAl set of these properties or traits but we’re usually just conceced with a given subset of traits for a gievn question

319
Q

What determines phenotypic varaition – ways that phenotypic variation can come about

A
  1. Genetic variation
  2. Environmental variation
  3. Gene X Envirnment interaction
320
Q

Genetic variation

A

Because we know someone’s genotype we can predict the phenotype

MEANS that phenotypic differences among individuals are epxlained by allelic differences (explained by genotypic differents)
- Phenotypic differences are a direct result of genotypic differences
- Straight fowards DNA –> Gene product = genetic variation

Example – varaition in human taste sensitivity

321
Q

Example of genetic varaition

A

Human tests sensitivity

Have PAV and AVI allele – the ability to detect compund = varies strongly with genotyoes
- The distribution of detecting the compound depends on the genotype

322
Q

Looking for which allele is homozygous

A

IMAGE

Answer: PAV because the heterozgous is more like the PAV that PTC homozygous
- Means that PAV is the driving phenotype

323
Q

Variation within each genotype (when looking at a trait that is genetic varaition)

A

Might still have more varaition within each genotype (same genetype and still different phenotypes – there is varaition that can’t be explained by genotype because they all have the same genotype)

Reason = might be that other genes affect the traut OR maybe have envirnmental variation too

324
Q

Genetic varaition inheritance

A

Genetic varaition = straightfoward inheritance between parents and offspring
- If you know the offsrping’s genotype then we can make a strong prediction about phenotypes

325
Q

Phenotype

A

Direct molecular product of the genome
- Straight fowards DNA –> Gene product

326
Q

Other examples of Genetic variation

A
  1. Eye color – likley predictable genotype
  2. Blood type –> only affected by genotype
    (very little possible effect of envirnment)
    • Purley genetic phenotypic varaitions (phenotype is the same regardless of envirnment)
327
Q

Common form of molecular phenotypes

A

Purpley genetoc phenotypic varaition (the phenotype is the same regardless of envirnment = often teh form of molecular phenotype)

328
Q

Environmental variation

A

Phenotypic differences among individuals are explained by difefrences in conditions
- Some envirnmnetal variable explains the differences in phenotypes
- Phenotypic differences exist due to differences in the conditions experinced by organisms
- Here – organisms can have the same genes BUT different phenotypes

Phenotype = dtermined by external condition (by extrinsic factor)

Ex. determined by diet or drug in an experiment

329
Q

How to know if it is envirnmental varaition

A

Hard to know:
- IF all the same genotype (like they atre clonal organsisms) but they are in different envirnemnst and have different phenotypes THEN it is likley an emvirnmental effect

IF they have the same genes BUT different phenotypes = based on envirnmnet

330
Q

Example of environmental variation

A

Daphnia – organism that reproduces by cloning (same genotype)

IF they are exposed to different environments THEN they look different
- Of they are reared around predators = they have a point and hard outside
- HERE – have different phenotyopes based on predator cues (based on envirnmental cues)

***They have the same gnotype BUT have different phenotyoes based on the envirnment

331
Q

Envirnmental varaition in humans

A

We have envirnmnetal varaitions in humans

Example – very muscular person –> based on diet + excersize

332
Q

Phenotypuc plasticity

A

Changes in the phenotype exhibited by the same genotype due to envirnmental differences
- Phenotype can be shaped by the envirnmnet BUT the genotype stays the same
- Envirnmental variation effects phenotype
- Envirnmental determines the phenotype

333
Q

What leads to phenotypic plascity

A

Envirnmental varaition

334
Q

Polyphenosim

A

Discerete phenotypic varaition arising from the same genotype in different envirnments (SAME GENOTYPE)
- Type of phenotypic plasticity
- Get catagorical varaition (one phenotype or the other) because of of different envirnments

Example – Daphnia (get either with body armore OR without – two discrete values)

335
Q

Polyphenisms vs. Non-polyphenism example

A

BOTH types of Phenotypoic PLasticity BUT only one is Polyphenism

Example #1 – Ants – Workers can be a range of body sizes based on theior diets as larva (continous gradient)
- Same genotype BUT different sizes depedning on how fed as larvae

Example #2 – Workers vs. soldier ants
- Depends on larval nutrition - ONLY have 2 forms = polyphenism

336
Q

Examples of Polyphenism

A

1 – Space toads
- Have 2 forms –> individuals will go one way or the other
- Have chnage in body size + change in trophic ecology (eating ecology)

2 – Tiger Salamnder
- Have two forms – some will go on land and some with stay in the pond
***Depends on the population density of the salamders in the pond (if there are many then they will leave the pond BUT if there are few then they will stay in the pond)

337
Q

Gene X Envirnment interactions

A

Means that the phenotypic differences that are caused by alleleic differences depends on. aparticular condition and vica versa (the differences cause my envirnment depends on a particular genotype)
- Effect of the allele depends on the envirnment or effct of envirnment depends on allele
- Phenotypic differences are driven by differnt intercations between alelleic varaitions and envirnmnetal conditions
- Genes have different effects in different envirnmnets

MEANS we don’t know the contribution of an allele to the phenotype without knowing the envirnment

338
Q

Means of interactions in GXE interaction

A

One thing depends on the other – effect of the genotype depends on envirnmnet and effect of envirnment depends on genotype

IS A statistical interaction – can’t predict the effect of the allele without knowing the envirnment

339
Q

Reaction norm

A

The mathematical relationship between environmental variable and the values at the phenotypic plastic trait (relationship between envirnment and phenotype)

In example – there is a linear relationship ebtween chemical and physiological response to pollutants (As the chemical concentarion increases the enzyme production increases)

340
Q

Example of phenotypic plastic trait

A

Phenotypically plastic ability to detoxify pollutants in environment
- Ability to produce detoxifying enzymes = costly (costs to up regulate those systems) = cost
- can be beneficual for the trait to be phenotypically plastic (if there is less pollutant then you dont upregaulte and if there is an increase in pollutant then you upregulate and shift to put more resources in)

In chart – as chemical concentration increases the enzyme production increases = phenotypic plasticty

341
Q

GXE interaction example

A

IMAGE – the two genotypes have different reaction norms = know that it is GXE because the effect of the envirnment depends on the genotyoe that you have
- The two lines intersect = means that they are not paraellel = means that the relatsionship between the envirnment and the phenotype depends on the genotype

In example – the slopes of the lines are different = they intersect –> we know that the relationship between phenotype and envirnment for one genotype is diferent form the other = know that the relstionship between the phenotype and envirnment depends on the genotype
- The envirnment afefcts each genotype differentlye = the affect of the envirnment depends on the genotype (DEPENDS = GXE)

***GXE because the two genotypes have different reaction norms

342
Q

How to know if there is a GXE interaction

A

In GXE = have different genotypes have different reaction norms
- The different reaction norms = evidence for GXE

343
Q

How to know if there is a GXE interaction

A

In GXE = have different genotypes have different reaction norms
- The different reaction norms = evidence for GXE

344
Q

Real world example of GXE

A

Seratonin Transporter gene:
- Based on variation in the transporter gene

SEEMS like the genotype affects depressive episodes BUT they found that the importance of the gene varies based on external conditions
- ALL of the genotypes have different reaction norms = the effect of the envirnment depends on the genotype = GXE (the affect of the allele depends on the envirnment that you are in – LIKE the affect of SS depends on the envirnment that you are in – all SS have different traits dependning on environment)
- ll = has very little effect on increasing probability BUT once have an S allele = increases the chance of a depressive episodes
- Increased chance depends on the genotype BUT the effect of that genotype depends on the envirnment

BOTH the genotype and the envirnment matters

OVERALL: genotypes have different reaction norms (all have different slopes) = GXE – because the effect of the gebnotype depends on the emnvirnment and each genotype is affected by the envirnment differentley

345
Q

Reaction norms + NS

A

Reaction norms = often the target of NS
- NS = acts on the reaction norm itself –> Act on the same enivrnments interaction with the phenotype
- Somtimes this can give the apperance of Lamarkian Phenomanon – because the change in evnirnment causes change in phenotype that is then pased down = seems genetic

346
Q

How do phenotyoically plastic traits evolove

A

By acting on the reaction norm

347
Q

Example of NS acting on reaction Norm

A

Mandica – Black worms can turn green after a heat shock treatment
- There are differences in the degrees of response of the catipillars = inidcate different reaction norms (because they each have have different leevls in plasticity – they turn different colors)
- The amount that temperature affects phenotype varies
- Have different phenotypic effects (some stay black + some go a little green and some go very green) –> IN ALL of the same temperatures they all they all respond differentley – they all trun different colors)

THEY ALL have different reaction norms because they all have different responses to the envirnment

Researchers made:
1. A high plastcity line
2. A control line
3. A low plasticty line (Stay black)

Results: The low plasticity line lost ability to turn green and the high plasticity line increased in plasticity

HOW – selection is acting on the reaction norm itself
- Low plsticity line = ends with lower RN
- High plasticity = ends with a higher reaction norm (means that it takes less temperature change in color)

***By selecting for envirnment determined traits = evolove because the reaction norm is chnaging

OVERALL – a selection experimnet on this GXE varaition not only chnages the phenotype but it does so by altering the reaction norm

348
Q

Reaction norm + plasticty

A

Low plasticty = lower reaction norm

High plasticity = Stronger reaction norm

349
Q

Normal reaction norms

A

Reaction norms are not usually linear

350
Q

What in reaction norm differs

A

Slope + shape + position of the reaction norm can differ by genotype

***The shape and the position can be under selection – that selection can change the reaction norm (can change the shape and the slope)

351
Q

Selection + reaction norm

A

The shape and the position can be under selection – that selection can change the shape and the slope

Selection = can change the shape – can go from being contibous to having only two options (from more gently sloping line to being either the value at the top or the bottom)

352
Q

Continous to polyphenism

A

Selection - can change the shape – can going from continous to only two options (from gently sloping tp being either value)

***Goes from continuous phenotypic plasticity to polyphenism – change the phenotypic outcome (because still phenotypic plasticity because change in phenotype based on environment but genotype isn;t change BUT only now have two phenotyoez

353
Q

Making a plastic trait fixed in a population

A

Selection on reaction norms can also take a plastic trait and make it fixed in a popultion (no longer repsonive to envirnment)

To make a genetically engrained chnage BY changing the sensity needed to be plastic

Ex. making calacous without needed any friction – At the start you need friction (need environmental change) to get them BUT can shift the amount of friction that is needed to be practically no friction needed = make an environmental variable into a fixed trait

354
Q

Genetic Assimiliation

A

The evolution of a fixed trait from phenotypic plastic varaition

***Was an envirnmental trait and is now hardwired

355
Q

What is needed to mkae it a fixed trait

A

To make it genetically engrained = changed by chnaging the sensity needed to be plastic

356
Q

How does Genetic Assimilation occurs

A

Occurs if you lower the limit of envirnmental condition needed
- If you make it so that you have the trait at. avery low limit of envirnmental condition then you will have the trait in all envirnmnets – in the end you have a varaible trait going to a genetically fixed trait

SINCE – lowered the limit and selection acted on the reaction norm – by pushing the infelction point of the reaction norm below the threshold – the trait will now appear under any set of realistic conditions

357
Q

Example of changing reaction norms

A

Salamander – reaction norm evoloved from something that was senistive to the envirnmnet to no longer behaving in a phanotypically plastic way
- IF you are in a big body of water then the salamnders don’t have to run away (because there is plemnty of space for them all to be in the water = can shift the reaction norm to make it less sensitive to chnage in phenotype)
NOW in all envirnments they stay in the wayer – a shirft in reaction nowm = no longer sensitive to change in envirnment
NOW they have the capacity to become terrestrial BUT they don’t because there was a chnage in reaction norm

***Increased envirnmental standards – it needs to be very dense for them to change = they are less sensiitive to change in envinrmnet = they won’t leave the water

358
Q

Range of mutations

A

Goes from small scale to large scale

359
Q

Small Scale mutations

A

Mutations that make a new allele at a locus in that gene

360
Q

Large Scale mutations

A

New variations that generate new loci
- Large scale or change in genome structure

361
Q

Example Small scale mutations

A
  1. Point mutations
    • SNPS
  2. Indels
362
Q

SNPS

A

Change in one nucleotide to another
Like a C → T – now have an A-T BP instead of a C-G BP

- Could change a codon = can change AA
 - Sequence length stays the same 

Worse case = 1 AA change

363
Q

Worse case SNP vs. Worse case Indel

A

Worse Case SNP = change in 1 AA

Worse canse Indel = screw up really bad

364
Q

Indels

A

Small inseration and deletions of base pairs

- Hard to know if mutation is an inseration or deletion
 - Some number of nucleotides are added or subtracted 
 - Chnage in length of sequnce
365
Q

When do Indels usually occurs

A

Usually occurs because you have a slip in the template – teh polymerases skip over = loss or gain BP

366
Q

Indels in the coding region

A

Shifts the reading frame –> Affects all. ofthe code downstream
- If in the coding region = all of the downstream is affected unless it is a 3 BP indel

***Causes severe change to protein

367
Q

Indels in Introns

A

Can affect splicing

***Indels almost anywhere can have an affect

368
Q

Mutations that we are concerned about

A

Most mutations that we are concerned with are mutations that are. inthe germ line (not somatic)

BECAUSE – somatic mutations are not inherited

369
Q

Germ line mutations vs. Somatic mutations

A

Somatic mutations ate not passed down but germiline are

DNA damage = drives germline and somatic but usually need error in the DNA repair mechanisms to have a germline mutations
- Damage in repair mechanisms = passed on

370
Q

Which type of mutations is more important for evolution? Point mutations in Exons (coding genes) Or Introns Or regulatory regions (promoters or suppressors – including cis and trans)

A

Debate = was debated for a while

Many say exons + some say regulatory regions (because then you might not make the protein)

ANSWER: ALL OF THEM ARE IMPOORTANT FOR EVOLUTION
Important alterations on small scale mutations can have an important effect

371
Q

Mutation is regulatory region

A

Might not make a protein at all

372
Q

Larger mutations

A

Might affect whole arm of a chromosomes OR might affect long noncoding RNA that is important in regulation

373
Q

Importance of long non-coding RNA

A

Important in regulation

374
Q

Small scale mutations make

A

Small scale muttaions make new alles within a locus

375
Q

Large scale mutations make

A

Large scale mutations generate new genes (New loci)

376
Q

Gene duplications are due to

A
  1. Unequal crossover (Meiotic error)
  2. retroposition
377
Q

Retroposition

A

mRNA processed by viral or retransponson machinery and integrated back into the genome
***More common that we think
- Often occurs after the RNA has been spliced then it is reverse transcribed into the genome
- Transcribed RNA gets picked up and gets reverse transcribed to DNA and integrated into the genome

378
Q

Retroposition process

A

Transcribed RNA gets picked up and gets reverse transcribed to DNA and integrated into the genome

***Can be inserted into the genome through DNA repair mechanisms

379
Q

Example of Unequal Cross over

A

Charlie- ____ Shark tooth disease –> Disease satte - due to liklihood of unequal crossover
- Because the CMT1A repeats on the sides can cause. tehchromsomes to not align correcvtley – crossover occurs so that you have 2 copies of a locus in one cell and no copies of the locus in the other celll

380
Q

Issue in Unequal Crossover

A

Crosover occurs so that you have 2 copies of a locus in one cell and no copies of that locus in teh other cell

NOW – get a longer and a shorter part
- Have too much ofa locus in 1 cell + Lose a copy of teh locus in the otehr cell

***Can cause phenotype – if the longer chromsome stays THEN new offspring might have extra copies of loci = the new loci can have new functions

IMAGE – start with all haveing 2 copies of exon 1 and 2 –> in the end one chromome that have 3 copies and 1 chdomsome with 1 copy

381
Q

Affect of Unequal Crossover

A

Can cause phenotype – if the longer chromsome stays THEN new offspring might have extra copies of loci = the new loci can have new functions

382
Q

Result of gene duplication events

A

Get novel Loci – Start with one loci and end with 2 loci (the 2 loci can have identical sequences)
- get new region of the genome

THESE 2 loci = now 2 genes because they are inherited independently of each other

383
Q

Where can Retrponson be inserted

A

Can be inserted into a copy fo. afunctioning gene

NOW – have 2 levels of affect
1. Get new gene
2. Break up another gene

384
Q

How do you identify Retroposition

A

Indeitified by one copy having exons and introns and the oyer copy somewhere else without the introns –> tells us it was inegrates again after splicing

SHOWS us that retroposition occured

385
Q

Retroposition + Expression

A

Might have a fully functional copy but it isn’t assocated with regulatory region of the gene that it came from – mighyt not be expressed at all of might be expressed differentley

386
Q

Trend in retroposition

A

New gene typically does not have introns – inserted after mRNA is spliced

387
Q

Where can gene jump to in retroposition

A

Can jump to new chromsome

388
Q

Chromosomal rearrangements

A
  1. Inversions
  2. Fissions/fussions

***Occur often

389
Q

Inversions

A

Change in the order of genes due to double stranded breaks and misaligned repairs – chang in the order of genes on chromsome

390
Q

Why does inversion occur

A

Due to mistake in DNA repair – if you have 2 breaks and the chromsome is twisted –> when the break is repaired = it can be attched back in a new way

391
Q

Importance of inversions

A
  1. They were some of the first “genes” studied in natural populations – Could study them because they are visible in the karytotype
    • They were studied before they could sequence DNA and just look in the micropscope –> teh inversions stood out – the two chromsoomes were no longer aligned = can be identofied in microscope
    • One of the first markers in molecular biology (looking at frequncey that this occurs)
  2. They are important for reconbination
392
Q

Inversion + Recombination

A

Inversions = important for recombination – chromsomes no longer can have recombinations
- Protects the region from recombinations – Makes genes linked –> if the genes are linked then Natural selection acts on them more. =acts on inversions more

393
Q

Natural selection + inversion

A

natural selection = acts on linked inversions – natural selection. =acts faster than individual genes inherited independeltley

NS = acts faster on linked genes than genes than genes that are inherited independetley. =NS acts on the inversion event because the genes are linked

***Inversions might play a strong role in evolutionary processes by keeping sets of genes together

394
Q

NS + linked genes

A

NS = acts faster on linked genes than genes than genes that are inherited independetley

***Seen in rapid evolution + Speciation

395
Q

Natural selection acting on Inversion

A

Having difefrent chromsomes based on the latitude – Natural selection acts on inversions in colder vs. warmer
- Example of a pattern of chromosomal adaptation
- NS = acts faster because multiple genes under selection together

396
Q

Importance of Fissions. +Fusions

A

Drives Karyotype diversity (Haploid chrsomosome counts)
- Number of chromsomes (haploid)

397
Q

Fission

A

1 Chromosome –> 2 chromosomes

398
Q

Fussion

A

2 chromosomes –> 1 chrossome

399
Q

Number of Chrosmome diversity

A

Organisms have a wide range of the amount of chrosmomes they have in one set (wide range in N)

Example – there are some organsims that have one gene per chromsomes. –have 16,000 chrosmomes

400
Q

How did we get 23 chromosomes

A

Our closest ancestor has 24 chromsomes – our 23 is bevcause of a fussion event

**Fusion event gave us our 23 chrosmomes
**
Shows that fussions/fissions drive karyotype diversity

401
Q

Whole genome duplication

A

Typically due to meitotic erros

Very common in some groups of organims (Particulaly plants)

May play a role in speciation and adaptation

May have been very important in early history of life – providing fodder for protein diveristy

402
Q

Whole genome diplication (process)

A

Have zygotes that end up with extra copy of genome (usually have diploid + diploid that are sually two haploids –> creates a tetraploid) –> That tetraploid individual acts like a dioploid with X2 chromsomes

403
Q

Importance of whole genome duplication

A
  1. May play a role in speciation
    • Important for speciation. inplamnts – makes sexually incomptaible plants)
  2. May have been very important in early history of life – providing a fodder for protein diveristy
    • Likley important for the biochemical paths that we have – the extra set of chromsomes due to duplication can mutate and evolve and take on new forms = important for developing complexity in Eukaryotic organisms
      • Think it was important for developinhg the complexity of Eukaryotic organisms
404
Q

How often do mutations occur

A

Occur pretty often – muttaions occuring in the germ line occur all of the time –> the DNA of the parents is different than the DNA of teh offspring

Because occur pretty often the fact that the DNA of the parents is almost always different that the DNA of the offspring is almost always true

***We can measure mutations rates by tracking lines of model organisms in the lab

405
Q

How do we know how often mutations occur

A

We can measure mutation rates by tracking lab lines of model organisms OR whole genome sequncing of known pedigree

Example Experimnet – Looked at the genome of parents vs. offspring (Sequnceing)
- RESULTS: had 49 ghermline mutations in one family and 35 germline mutations in another family
- The two families differeed because in one the mutations mostly came from father and in one the mutations mostly came from the mother

SHOWS – mutations almost always occur but how it ends up differs from person to person (Ex. in some cases the mutations might come from the mother and in some the mutations might come from the father)

406
Q

What mutations are of interst

A

Germline mutations – because those of able to be passed down (those are heretible)

407
Q

Mutations rates across organisms

A

Differs from organism to organism

408
Q

Mutation rate at. asingle locus Vs. mutation rate in organism

A

The chance of a mutation at a single locus is low BUT if you scale that up to account for all of the loci in a genome get a liklihood of having of 30 mutations

The chance of a mutations at a singel nucleotide is low but when you scale the chance of a mutation up to genome level = epxevct to see around 30 mutations in the genome level

IMAGE – shows mutations rates for a single locus

409
Q

Mutation rates within the genome

A

Different regions of the genome have different mutation rates

Example – mitocondria mutation rate is higher than the nuclear genome

410
Q

Variability in mutation rate

A

Mutation rates are very variable BOTh acrosses organisms + within organisms but between regions of the genome

411
Q

What do most mutations do to fitness

A

The majority are either bad or neutral (no effect on fitness) BUT some can imporve fitness
- beneficiual miutations are rare but do occur

SEEN IN bacteria + Yeast
- Studies look at the fitness of clonal indivioduals vs. the fitness of the ancestral strain
- Most common = nuetral
- In the chart most of the mutations. are<1.0 – means that they lower fitness or at 1.0 which means that they are neutral
- The chart also shows that some of the mutatinos were lethal (biggest decrease in fitness)
- YEAST = mostly nuetral with some distribution of deleterious + have lethal
- BUT in both organisms there are sine numbers >1.0 – means that there is. anincrease in fitness = have 3-4 mutations that impirved fitness over ancestral

412
Q

Consequence of mutations

A

The mixture of bad BUT also some good mutations still provides enough fodder for NS

***Can see in a mutation Accumilation experiment

413
Q

Mutation Accumilation Exeperiment

A

IF mutation just acted by itself (doing a mutation accumulation experiment) – allow mutations to build up but take selection out of the picture by babying the warms as much as possible – the warms are not completing at all

RESULTS – After genertaions the fitness. ofthis line decreases A LOT
- When there is No natural selection (because took out any competition) + have a lot of mutations the fitness decreases –> the new mutations are deleterious – as they accumilate theu hurt fitness

IF intriduce natural selection (increase NS – Increase competition) –> The Naturak selection can sort through allelic varaition
- NS = can pick out the good mutations and take out. thebad mutations and return the popultion to orginal fitness
- returns very quickly to normal fitness

OVERALL – is NS is not acting then mutations lead to decrease in fitness BUT when NS is restored it can act efficiently and restore the fitness alsmot instantaneously

414
Q

Mutations + fitness

A

In the absence of selection, deleterious mutations
accumulate and drive fitness down

Return of selection: rapidly sort out the good from the
bad and fitness bounces back

415
Q

Textbook definition of Pop Gen

A

The branch of evolutionary biology responsible for investigating process that cause changes in allele and genotype frequencies in populations

ISSUE with definition – Evolution = the change in allele frequncey = all of evolutionary biology should look. atchnage in allele frequcney BUT this syas that Pop gen. isa branch of Evolutionary Biology = not a good definition
- Incorrect in saying that it. isa subset of evolutionary biology because it is really all of evolutionary biology – all of Evolutionary biology needs to look through this lense
- Really all of evolutionary biology needs to boil down to pop gen

416
Q

Population Genetics (good definition)

A

The mathematical and empirical study of allelic variation
within and among populations, including the dynamics of changes in allelic variation through time

***All about understanding allele frequcney

417
Q

Why is it important to study Pop Gen

A

Understand population geentics = impotant applied applications + important for looking at postulates forms

Example – Affects forensics – need to know gentics and allele frequencies to do forensics

Important because:
1. Mechanistic underpinnings of evolutionary change (or stasis)
2. Understanding Pop Gen is essential to a number of applied fields and it has strong implications for fields outside of evolutionary biology

418
Q

Allele

A

Varaint forms at a genetic locus

419
Q

Frequency

A

Looking at something in terms of the proportion

Looking at the counts relative to the whole
- Looking at the proportion of varaition for a locus represented by as ingle allele

Count of an allele/WHOLE (count of all alleles in population)

420
Q

Example frequency (using phenotype) – 21 Students with glasses and a total of 157 students – What is the Frequency of students with glasses and without glasses

A

Frequencey of students with glasses = 21/157 = 0.134

Frequency of studnets without glasses = 1- 0.134 = 0.866

**Can just subtract from one because we know that the two possible Frequency need to add up to one

421
Q

Adding up frequencies

A

All of the individual frequencies will ALWAYS add up to one (IF have FReq 1 and Freq 2)

Freq 1 + Freq2 = 1.0

OR if have two alleles A and a
Frequencey of A + freq of a = 1.0
NO MATTER HOW MANY ALLELES THERE ARE – ALL OF THE ALLLES NEED TO ADD UP TO 1.0
- Same is true for genotype frequencey

422
Q

Finding allele Frequency

A

Work the same way as phenotype Frequency – need to count up all of the allele in question and determine the proportion it makes up of all of the copies of that locus in the population
- Look at allle and determine the proportion that they make up of all of the alleles

423
Q

Example – Finding allele Frequency

A

of homozygous Indv + 1/2(# of heterozygous Invd)/Total number of individuals

Have two alleles A and a

Can count – we know that the total number of individuals is 147 (can just add up all of the individuals in the chart)

Need to find the frequencey of A:
– Might want to do 47/147 –> THAT IS WRONG – because these are not allele counts they are genotype frequnceies – need allele count + need to account for how alleles are distrubuted into the genotypes

Focusing on A:
47 AA –> 47 A and 47A –> 94 A
88 Aa –> 88 A and 88 a
12 aa –> 12 a and 12 a –> 24 a
***Need to double to account for being diploid + need to adjust for heterozygous
Total A = 94 + 88 = 182 A
Total A/ Total Alleles = 182/294 = 0.619

OTHER WAY:
***Instead of counting alleles we can count genotyoes and adjust accordingly
# of homozygous Indv + 1/2(# of heterozygous Invd)/Total number of individuals

47 + 1/2(88) / 147 = 0.619 –> get. thesame answer

OR – can use genotype frequencies
Freq of A = Freq of AA + 1/2(Freq Aa)
0.319 + 1/2 (0.599) = 0.619
***Here = don’t divide by anything because already in frequencies

Looking at a:
12 + 1/2(88) = 0.381

OR

1.0 - 0.619 = 0.381
- can do this because freq of A + Freq of a (because the sum of all of the frequencies of all of. thealleles in a popultion = 1.0) = 1.0 (need to sum up to one)

424
Q

Finding the total number of indoviduals

A

Just add up all of the genotype frequencies – because each individual has one genotype

AA - 47
Aa - 88
aa - 12

of indiviudals = 47 + 88 + 12

425
Q

Why is genotype freqincey not allele frequencey

A

Allle count is NOT the genotype frequincey becasue each genotype has two alelles (because these are diploid organisms) – have two alleles per locus (two alleles per genotype)
- When you have diploid individuals – total # of alelles = X2 the number of indivoduals

Example. –147 indiviuals –> there are 294 copies of the locus

NEED TO ACCOUNT FOR HOW ALLELES ARE DISTRIBUTED IN THE GENOYTYPES (need to account for heterozygotes) + Need to account for diploid nature

426
Q

Equation for calculating allele frequency from genotypes

A

of homozygous Indv + 1/2(# of heterozygous Invd)/Total number of individuals
- Use 1/2 because only 1/2 of the heterozygous are each of the alleles (1/2 A and 1/2 a)

Instead of counting alleles we can count genotyoes and adjust accordingly

OR
You can work directley with genotype frequnceies
***Genotype frequncies also all have to sum to 1.0
Freq A = Freq of AA + 1/(Freq of Aa) – here you don’t divide by total individuals becvaue you ate already using frequnceies
- By dealing with genotype frequencies we have already accounted for the proportion of the whole = no need to divide anymore

427
Q

Finding allele frequencey from genotype freunecey

A

Freq A = FreqAA + 1/2Freq of Aa

Example
AA –> 47/147 = 0.314

Aa -> 88/147 = 0.599

aa –> 12/147 = 0.082

Freq A = 0.314 + 1/(0.599) = 0.619

***Don’t divide by anything here because they are already in frequcneies

428
Q

Sum of all of the frequencies of all the different alleles in a population

A

Equals 1.0

429
Q

How to get genotype frequencey

A

of indioviual with genotype/ Total # of individuals
***No need to double here (Just number/total)

Ex.
#AA/Total # of individuklas

430
Q

Practice –

A

Freq H+ = 0.8

Freq H- = 0.2

Genotype Freq:
HH = 0.63
Hh = 0.34
hh = 0.03

Freq H+ = Freq of HH + 1/2 Freq of Hh
0.63 + 1/2(0.34) = 0.8

Freq of h = 1.0 - 0.8 = 0.2

431
Q

Population

A

A group of interbreeding individuals and their offspring (for sexually reproducing organisms)
- Hard to define

More generally:
Perhaps more generally: a group of conspecific
organisms occupying a more or less well defined
geographic area that exhibit reproductive continuity from generation to generation
- Conspecific = members of the same species
- We model reproductive continuity –> potential for allle frequncey to change from one generation to the next (parent genotype to offspring genotype without the input from other groups)

432
Q

What are we modelling in Pop Gen

A

We model reproductive continuity –> potential for allle frequncey to change from one generation to the next (parent genotype to offspring genotype without the input from other groups)

433
Q

Mendle’s laws in populations

A

We need to think about how Mendle’s Laws operate at the population level from one generation to the next
- Sclaing up Mendle’s laws of segregation and independent assortment up to the popultion level

KEY = thinkning about reproductive continuity (offspring genotypes)

434
Q

What is needed when scaling up mendelian principals up to populations

A
  1. We have to define the specific life cycle of our populations
  2. Examine the points at which allele frequencies might be subject to change

NEED to think how allele frequncies might chnage from one genration to the next – need. tothink about this chnage in a life cycle

435
Q

General Life cylce that we use

A

1 – ADults –> Sdults make gametes – make up the gene pool (2) –> Gametes form the gene pool combine to make zygotes (3) –> Zygotes mature to offspring (these new offspring make up. thepopulation) (4) –> Offspring become adults (1)

  1. Parental genertaion
  2. Gametes pool derived from the parental generation
  3. Combination of gametes from pool of zygotes
  4. Offspring generation
436
Q

Allle Frequncies within life cylce

A
437
Q

What types of populations do we use in our models

A

We use “idealized populations” – a simplified model of a population that meets certain criteria assumptions –> allowing us to islate the effects of interst

REAL groups of organisms might not meet this BUT this allows us to islate the effects of interst

DOING SO = gives us a NULL model –> Shows. us the way we think the world works and then compare that to hwat actually happens
- We can compare data from real populations to expectation from idealized populations to test hypothesis

438
Q

Example – Scaling up mendelian Principlas in populations

A

1 – Start with our parental popultions –> genotype the indoviuals – get the genotype frequencies for parental generation

GET Parents popultion genotype frequencey
Example:
AA =0.36
Aa = 0.48
aa = 0.16

2 - Generate the gamete pool – based on. theintial parental genotypes
- Get the frequencey of the alleles in the gamete pool
- Assuming Mendle’s kaws = take a diploid genotype and make all of the possible gametes

Frequncey of gametes = Frequncey of alleles on the parental generation

Freq A = Freq AA + 1/2(Freq of Aa) = 0.36 + 1/2(0.24) = 0.6

Freq A = 0.6
Frq a = 0.4

Freq in gametes = 0.6 and 0.4
- means that 60% of sperm is A and 40% of sperm. is a and 60% of eggs are A and 40% of eggs are a

Can call Freq of A “p”; Frequncey of a “q”
P + q = 1.0 (Freq of A + Freq of a) = 1.0
q = 1 - 0.4 –> q = 0.4

NOW = we know that the gamete pool is 60% A and 40% a

3 – Geenrate Zygotes
- use basic probability – choosing one sperm and one egg at random from the gamete pool
- Porbability of getting a gamete with a particular allele is simply equal to the allele frequncey
- probability of choosing a gamete with A = freq of Ain gemete pool

P(A sperm) = p = 0.6
P( a sperm) = q = 0.4
P(A egg) = p = = 0.6
P(a Egg) = q = 0.4

P(A sperm) And P(A egg) = 0.6 X 0.6 = 0.35 –> P(AA) = 0.36
SAME AS p X p = 0.36

P(aa) = 0.4 X 0.4 = 0.16
q X q = 0.16

P(Aa) = P(A sperm) AND P(a Egg) OR P(a sperm) AND P(A Egg)
- There. aretwo ways that this can happen = need to account for both
P(Aa) = [0.6 X 0.4] + [0.4 X 0.6] = 2[0.4 X 0.6] = 0.48
[p X q] + [q X p]

4 – Assuming that all of the zygotes survive and develope – the genotype frequncies of. tehnew generation are

AA = 0.36
Aa = 0.48
aa = 0.16

NOTICE: NO CHANGE – the same frequncey as the parental generation
- Genotype -> gamete frequncey –> Probability events in teh gamete pool –> zygoites –> if all of the zygotes surivive to be offspring = the genotyp[e frequnceies don’t chnage in the offspring

439
Q

How do you get the frequncey of gametes in gamete pool?

A

You can asusme mendles laws – take a diploid genotype and make all of the possible gametes
- Get the gamete pool from the parental genotypes
- Want the alleles frequncey on the gamete pool – this is equal to teh allele frequncey in parental generation

END – frequencey of gametes = frequncey of alleles in the parental generation
- If we make the assumption that all individuals in the parent population contribute evenly to the next population –applying Mendel’s law of segregation
to the population as a whole –> Frequency of gametes equals allele frequency of the parental population

440
Q

P

A

The allele frequncey of the alelle that we are focused on

***Could be an allele that doesn’t even make a phenotype
- Doesn’t say anything about dominant vs. recessive

***In an idelaized biallelec system = we can call the frequncey of the other allele “q”

441
Q

Generating zygotes from the gamete pool

A

Use Basic probability – choosing one sperm
and one egg at random from the gamete
pool
- probability of choosing a gamete with A = freq of A in gemete pool

Probability of getting a gamete with a particular allele is simply equal to the allele frequncey in gamete pool

442
Q

Probability of two independent events

A

Probability of two independent events
occurring together is the product of their
individual probabilities

AND statement = multiply

443
Q

Probability of two ME events

A

Probability of either of two mutually
exclusive events occurring is the sum of
their individual probabilities

OR statement = ADD

444
Q

Looking at Punnet square for a population Vs. for two individuals

A

Started – punnet square of two individuals (just looked at male and female)
- Here – the frequency of each of the gametes is 50% (50% chnace they will give A and 50% chance they will give a)
- HERE – P and Q = 50%
- If only two inidviuals then p and q = 50%

THEN – just change cross to have different frequency of p and q to account for all indivdiuals in the population (NOW just chnaging the cross to have different requencey of p and q)

NOW – instead of a gamete pool of two indoviduals – gamete pool is of the entire idealized popultion
- Have new p. and q values to account for allele frequencey. inthe gamete pool

THEN – can use p and q in. thepunnet square –> The frequncey of each genotype in each square is equal to the pdorct of the gamate (allele) frequencies
- Have AA = p X P
- Have aa = q X q
- Have Aa = p Xq OR q X P = 2pq

END – know that p^2 + q^2 + 2pq = accounts for all indovoduals in the popultions = p^2 + 2pq + q^2 = 1.0

445
Q

Looking at Punnet square for a population Vs. for two individuals

A

Started – punnet square of two individuals (just looked at male and female)
- Here – the frequency of each of the gametes is 50% (50% chnace they will give A and 50% chance they will give a)
- HERE – P and Q = 50%
- If only two inidviuals then p and q = 50%

THEN – just change cross to have different frequency of p and q to account for all indivdiuals in the population (NOW just chnaging the cross to have different requencey of p and q)

NOW – instead of a gamete pool of two indoviduals – gamete pool is of the entire idealized popultion
- Have new p. and q values to account for allele frequencey. inthe gamete pool

THEN – can use p and q in. thepunnet square –> The frequncey of each genotype in each square is equal to the pdorct of the gamate (allele) frequencies
- Have AA = p X P
- Have aa = q X q
- Have Aa = p Xq OR q X P = 2pq

END – know that p^2 + q^2 + 2pq = accounts for all indovoduals in the popultions = p^2 + 2pq + q^2 = 1.0

446
Q

Hardy-Weinburg Equillibrium

A

P^2 + 2pq + q^2 = 1.0
- Sum need to always equal 1.0 – accounts for all genotypes
- Looks at allele frequencey and the porbability of an allele in the gamete pool

CAN BE SEEN IN PUNNET SQUARE – look at image
- They ALL have to equal the whole rectangle = no matter what they always add up to 1

447
Q

How do we know if a population is in equilibrium

A

Look if the genotype frequnceies matches the allele frequncies

NO MATTER WHAT – the sum of genotype frequncies should still add to 1

448
Q

Getting H-W from Punnet Square

A

You can make the punnet square with the allele frequncey of each allele – include p and q

THEN you can see that:
Freq AA – PXP = p^2
Freq Aa – P X q OR Q X P = 2PQ
Freq aa = q X q

***Can do frequnceies in this way because the frequncie of AA = Freq of A AND the Freq of A = P X P

ALL OF THESE NEED TO ACCOUNT FOR GENOTYPES OF ALL INDIVUDALS IN POPULTIONS = ALL ADD UP TO 1

GET EQUATION – P^2 + 2pq + q^2 = 1.0

449
Q

Assumptions of the H-W model

A
  1. No selection
  2. No mutation
  3. No migration (in or out)
  4. Infinate popultion size
  5. Mating choice occurs at random

Violating 1-4 = changes allele frequncies = generates evolution

450
Q

What happens if violate random mating

A

Violating random mating assumtion DOES NOT change allele frequencies – only changes genotype frequencies

=

451
Q

Purpose of infinate population size assumtion

A

Important assumtion that genetic drift is based on

SMALLER populations = have inevitability of chnage in allele frequency

***Makes this an idealized model

452
Q

Where can we examine for fitness in life cycle

A

We can look at different points in the life cycle fir fitness – can exmaine fitness at many time points
- Can consider each point individuals

One can model the seperarte components. offutness at different points along our generlized life cycle
- ALL of the seperate fitnesses these typically all sum together to one value of overall fitness that we would use to adjust our HW model

Examples = in image

WE will just look at survival for fitness BUT you can incorporate other metrics of fitness into the models – it’s generally easier to think about, we’re also going to stick with examples where fitness is driven by differential survival rates
- All of the ways to look at fitness sum together but we will look at one alone
- We will just look at different survival rates
- Assign fitness value to genotyoes based on differential survival

453
Q

Selection

A

Essentially unequal rate. ofsurvival and reproductive success acriss genotypes

454
Q

Quantifying seleectin

A

Requires Quantifying unequal survival and reproduction

455
Q

w

A

Generalized fitness value

456
Q

p and q in non-dominent/recessive relationships

A

You can still use p and q – doesn’t matter which you call p and which you call q
- p and q say nothing about dom/rec

p = just the one that we are ficusing on

457
Q

Assigning fitness. inour class

A

We will just asisgn fitness value to genotypes based on different survival
- Looking at survival rates and assign fitness

WE look at juvinile to adult hood part of life cycle (differences in survival to reproduction)

458
Q

Quantifying fitness

A

Example – we have moved mice to. a location were coat color matters
Moved 1000 mice from a population in HW to a new location

We are looking to see if coat color is under selection (looking at ciat color)

Total = have 1000 mice –> tracking their survival in nature
- Intital population is in H-W (gene frequenceies match expenctations –> NOW putting mice in new envirnment)

Here
AA = 0.36
Aa = 0.48
aa = 0.16

THEN before reproduction a number of mice are eaten
AA Survivnng = 288
Aa Surviving. =288
aa Suriving = 64

OVERALL – need to compare the observed survival rate vs. the expected survival rate (expected = that each have equal survival rates)

Steps:
1. Need to calculate the survival rate for each geneotype
- Ratio of mice survivors in each genotype vs. the expected number of survival if Survival is uniform

  1. Need to calulatue NULL – that survival rate is uniform
    - To find – take total suvivors in population/ total in populations

288 + 288 + 64 = 640 –> 640/1000
P(survival) = 0.64 – if it is unifrm

THEN need. to find teh expected NUmber of survivors per genotypes (if survival rate is equal)

Expected number = Number of genotype X P(survival in unofrm)
- Exoect 64% survival in each genotype IF survival is uniform (expect 64% of each genotype to survive to reproduction)

0.64 X 360 = 230.4 – expected numbver of survivors
0.64 X 480 = 307.2
0.64 X 160 = 102.4

NOW have expected survivors

  1. Comprare observed vs. Expected survicors
    AA – 288/230.4 = 1.25
    Aa – 288/307.2 = 0.9375
    64/102/4 = 0.625

THESE numbers = represent the deviation form uniform suvrival for each genotype –> Theyre propeortional over or under the representation of that genotypoes in the next geenration = they are fitness
- They show the deveioation from unoform surivale (If uniform survivale is 1 then AA has slightly higher survival and Aa has slightly lower survival)

THIS GIVES ABSOLUTE FITNESS BUT we want theor relationships to each other –>. wecan rescale them (we don’t want to use the raw fitnes svalue we want them on a relationship scale– want relative fitness)

THEN TO GET RELATIVE FITNESS – We can do this by simply setting the value of the highest
fitness genotype to 1 and dividing the others by that value to adjust them accordingly

Mke your highest values = 1 and dvide. therest by that value
Here :
1.25 is highest –> 1.25/1.25 = 1
0.9375/1.25 = 0.75
0.625/1.25 = 0.5

NOW have relative fitness

459
Q

Adjusting H-W model

A

Before = we used an idealized model 00 no differentail survival or reproduction (just random events) –> This kept frequencey the same
- Mice were not evolving
- They were NOT under selection

NOW – we are putting them under selection

460
Q

Mice + coat color studies

A

This system has been studies a lot

Mice = get eatne by Hawks and hawks are visual predators – coat colro allows some mice to blend = allows for differential survival
- Look at survival of mice. inreal studies in nature + done with fake mice and looking at attack rates

461
Q

What is needed to quantify survival

A

Need to see if the survival is uniformly or not uniformly distributed for each
- Need to see if the survival rate for each as a null model that each have equal survival

Need to compare expected to observed survival
- Need to look at the ratio of mice surviving in each genotype compared to expected number. ifthe survival rate is uniform

462
Q

Calculating Null for quantofying survival rate

A

Null = that survival rate is uniform
- That they all have

Do total amont of surivvors in populations (regardless of genotypes)/Total populations

463
Q

Meaning of survival rates

A

If over 1 = means that that genotype is slightly more liley to survive

If less than. 1= means that genotypes is lsightly less likley tp survive

Ex. 0.625 – means thaty you have a 0.625 chnace. ofsurvival relative top everyone else in the same popultion

464
Q

Why go from absolute fitness to relative fitness

A

Because we care about their relationships to each other

DO this. byseeting the highest fitnes sto 1 and rescaling everything relative to that

465
Q
A
466
Q

How to predict effect of NAtural selection from. onegeneration to another

A

You need =fitness BUT you also need to think about it in the context of teh current popultion – need to know the starting point of the popultion for alelleic variation
- The effect of natural selection doesn’t just
depend on these values alone, it depends on
the context of the allelic variation in the
population too

NEED
1. Relative fitness
2. Need starting alelelic frequncey

Need to know fitness + allele frequncey THEN you can know if Natural selection is acting by itself

THEn you need to know the avergage fitness. ofthe populations as a whole – how high or below avergae fitness are you if you are carrying a certain phenotype

467
Q

What effects whether an allele will increase or decrease

A

Depends on the genotype fitness values and. the current allele frequnceies in the popularions

NEED – to calculate for avergage fitness across the popultions – the avergae fitness takes both alelleic frequencey and fitness into account

What alleles will do depends on Avergage fitness (w/)

468
Q

Average fitmess in populations

A

Takes into account allelic frequencey and and realtive fitness

YOU COULD – add all of. thefitness of all of the indivuduals in populations and divide by the total BUT you can just use genotype or allele frequncey
- If you know allele frequncey and fitness = know Avergage fitness

w/ = P^2wAA + 2pqwAa + q^2waa
In example – w/ = 0.8

469
Q

Calculating effect of natural selection

A

NEED:
1. Avergage fitness
2. Starting allele frequnceies

Using w/ and relative fitness and allele frequncey = can calulate what alleles frequncey will be from. onegeneration to the next

LOOK AT THE CHANGE in allelE FREQUNCEY

dP = p/w/ X [(PXwAA) + (q X wAa) - w/]

Example – (0.6 X1) – means that you have a fitness of 1 60% of the time – are above w/ 60% of the time

(0.4 X 0.75) – means that you have a fitness of 0.74 40% of the time

IF dp = 0.075 – tell us that teh allele frequncey will be slightly higher in the next generation
p’ (p in next generation) = 0.675 – alelle frequncey in the next generation

470
Q

Effect of natural selection

A

The change in allele frequceney between the parental and offspring generation

471
Q

Avergage excess

A

[(PXwAA) + (q X wAa) - w/] – average fitness effect of a gamete carrying allele A – that can combine at random with either A or a gametes in the population at their given frequencies

A gamete can either combine with another A – then get AA OR can combine with a and get Aa –> depedning on which happens have diffrent affects on fitness (if AA – has certain fitness + if Aa has different fitness then subtrcat that from the avergae fitness)
- If you have A in the gamete pool = can form zygote with. Aor a – look. atthe probability that you will get AA or Aa – done by multiplying by. p and q
THEN once you have the expected amount of AA or Aa you can see if on avergaege You will be above or below w/ by subtracting from w/
- SHows tha orbability of A combining with A and the fitness that the resulting zygote would have
WHETHER AN ELLE GOES UP OR DOWN IS BASED ON AVERAGE EXCESS

472
Q

Relationship between p and q change

A

If p increases by a certain amount q will decrease by that same amount

If p increases by 0.075 then q decreased by 0.075

LOGICAL - because p and q always add to 1

473
Q

How should the lowest fitness allele change

A

The lowest fitness allele should go down because its the lowest fitness

Highest fitness alelle should go up

474
Q

Selection coeffeciants

A

Sometimes it is easier to keep track of the strength of selection directley rather than relative fitness
- Look at selection directley
s = 0 – no sleection aganist it

s (selection coefficient) = 1 - Relative fitness

475
Q

Graphing popultion fitness

A

Preidcting the outcome of NS

LOOKING at mean popultion fitness vs. allele frequncey (w/ as a function of alle frequcey for a particular set of fitness values)
- Tells you w/ at a certain allele frequncey

When picking points always pick p = 0 and p = 1
Example:
1 Point – p = 0 –> w/ = 0.5 (because at p = 0 then ONLY have q –> W at aa = 0.5)

2 point – p=1 –> w/= 1 (AA = 1)
- If the entire popul;atioon is A then p=1 –> Then everyone has w = 1 –> then w/ = 1
- If fixed for A then w/ = 1

3 point – p= 0.5
CAN use equal;toon to find w/ at p=0.5 BUT here since Homozygous is Dom is. 1and Homozygous rec is 0.5 THEN you know that w/ of 0.5 would be in the middle of them = w/ would be 0.75 (Can’t always do it this way but can always use the equation)

476
Q

How many points do you need in graphing population fitness

A

Need 3 points in plot (shows if the graph is a staight line or has curves)

477
Q

Effect of Adaptive topography on a population

A

Efefct of NS = always to push the graoh uphill
- Want the max w/ based on ale;les in popultion – NS push popultion uphill
- w/ will increase uphill as much. aspossible
- Shows how adaptation will occur over adapative Topograohy

NS will always push the population uphill along the topography

Example (from the calculations earlier)
If have p = 0.6 –> w/ = 0.8 – in teh next geenration when p = 0.675 w/ becaomes 0.8375 (Shows that NS is pushing AT uphill)

478
Q

Graphs of fitness vs. alelle frequncey

A

Adaptive topograohy

USE the graogs to define an adaptive topography for the popultion

479
Q

Linear Adaptive topography

A

If linear slope – affect in w/ for a give chnage in dP – rate of increase is the same

480
Q

Example graphing Adaptive topography

A

Solving for the middle point:

Pick p=0.5 –> and the plug in to w/ –> get w/

HERE – NOT a styraight line
- w/ will still always go up hill BUT here NS is pushing P to decrease
- Curvature = affectes the rate at which this happens

Lower slope = smaller chnage in fitmess (lower investment)

Steeper slope = small chnage in P leads to bigger chnage in w/ (higher investment)

481
Q

Steepness in Adaptive topography

A

Steepness of the slope determines. thestrenbgth of affect of Anatural selection

Lower slope = lower investment (Making less of a change when putting. ineffort)

Steeper slope = small chnage in P leads to bigger chnage in w/ (higher investment)

482
Q

Fitness differential + NS

A

NS can work on any fitness differential – in the absence of other evolutionary forceses

Weaker fitness differences just lead to slower rates of change

ALL = end with fixing for one allele and gegtting rid of the ither – occurs in any case of selection even if diffrence in fitness is not as big

No matter the strebgth. ofNS = still change alleles – The strength of selection just alters the rate (just takes different amounts of time)

ALSO no matter the diffreential – the slopes of the lines (the fastest rate of chnage) = al;ways when p=0.5 – when the genetic varaition in fitness is at its highest

483
Q

Effect of NS

A

Directional selection – always pushes to get rid of one and have only the other

484
Q

Where does allele frequencey change the fastest

A

Looking. atthe slop of chnage in alelle frequncey over time – where it chnages the fastest = always in the middle
- rate. ofchnage os fastest at 0.5 – because at 0.5 is where you have the most varaition

RATE OF CHNAGE IS PROPORTIONAL TO THE AMOUNT OF VARIATION

485
Q

Fisher’s Fundamental Theorem of Natural Selection

A

Change in population fitness is proportional to
the variance in fitness

Rate of chnage = the fatsest at p=0.5 – fastest when there is the most variation

486
Q

Natural Selection is a…

A

Natural Selection is a deterministic force – if we know what the conditions are, we know what the outcome will be
- Natural selection by itself is driven by straight forward mathematics towards a predictable outcome