Test #1 Review 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

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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5
Q

Key Developments before Darwin

A
  1. Antiquity of the world
  2. The relationships among organisms
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6
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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7
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

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8
Q

Lamark’s heredity

A

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

***HAD IDEA OF AQUIRED INHERTIANCE

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9
Q

Lamarkism

A

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

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10
Q

How do we know that Darwin’s conclusion were inevtiable

A

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

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11
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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12
Q

Componenets of Darwinian Evolution

A
  1. Pattern
  2. process
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13
Q

Pattern of Darwinian Evolution

A

Common decent – Descent with modification

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14
Q

Process of Darwinian Evolution

A

Mechanisms for how changes arrive – process = natrual selection

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15
Q

Two models for explaining patterns of biodiversity

A
  1. Special Creation
  2. Descent with Modification
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16
Q

Special Creation

A
  1. Species are immutable (unchnaging)
  2. Lineages fo NOt diverge
  3. Species are created seperatley
  4. Species are geniologically independet – not fundementally realted to each other
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17
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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18
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

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19
Q

How do we make species change

A

We domesticate things = we know that species change over time

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20
Q

Evidence of species changing over time

A
  1. Artifcial Selection
  2. Applied Breeding (domestication)
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21
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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22
Q

Does speciation occur?

A

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

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23
Q

Speciation

A

One lineage splits into two seperate lineages

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24
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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25
Q

Law of Succession

A

Correspondance among fossils and existing fauna and flora in spaces

***Evidence that new forms arise from old -
Example #1 – Australian fossils that are mammals are marsupials BUT asiam mammals are placentals

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26
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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27
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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28
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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29
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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30
Q

Evidence that different groups of organisms are related

A
  1. Homology
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31
Q

Places homology is seen

A
  1. Vestigal traits
  2. Atavism
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32
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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33
Q

Psudogenes

A

Non-functional copies of coding genes Example – Vitamen C synthesis in Primates

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34
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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35
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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36
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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37
Q

Orthologs

A

Homolgous genes between species – across species

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38
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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39
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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40
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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41
Q

Malthus (overall)

A

Was one of the first people to really think about teh mathamatic reality of human demography - He realized the remarkable power of unchecked population growth

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42
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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43
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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44
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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45
Q

Geometric/Exponential growth

A

Population is increasing by constant rate per individual over time

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46
Q

Arithmetic growth

A

Population increase by a constant amount over time

***this does not take into account the density of the population

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47
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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48
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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49
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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50
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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51
Q

What stops us from being in a state of catastrophe

A

Mortaloty rates stop us from being in a state of 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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52
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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53
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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54
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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55
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

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56
Q

Where can variation be seen?

A
  1. Seen in human popultions – Example is disribution of height (
  2. See genetic variation within popultion – can see varaition in genome
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57
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

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58
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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59
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

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60
Q

Why is postulate #2 hard to measure?

A

Because heretibility is complicated

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61
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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62
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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63
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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64
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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65
Q

Most important postulate

A

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

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66
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
- 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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67
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

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68
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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69
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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70
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 test3 – Do all flies continue to the next generation – is there variability in survivorship – YES4 – 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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71
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 2. 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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72
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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73
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

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74
Q

Darwinian Fitness

A

The extent to which an individual contributes to future generations
***Need to think of it in terms of LIFETIME reproductive output

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75
Q

Survival + Fitness

A

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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76
Q

What is needed for fitness

A
  1. Survival
  2. Reproduction
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77
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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78
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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79
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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80
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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81
Q

When can population evolove

A

If the 4 postulates are trie

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82
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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83
Q

Misconceptions about evolution

A
  1. individuals evolve – REALITY = selection acts on individuals BUT individuals don’t evolove2. Natural sleection can see into the future – it cannot3. Selection adds more varaition – REALITY is that selection acts on existing varaition in popultions4. Selection results in perfection – NOT TRUE 5. Selection favors complexity – NOT TRUE6. Being evolutionarily advancd – subjective
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84
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

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85
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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86
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

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87
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

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88
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

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89
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
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90
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

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91
Q

Selection + Perfection

A

Selection does NOT result in perfection

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

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92
Q

Selection + Complexity

A

Selection DOES NOT favor coplexity – life has increased in complexity iver time BUT NOT because selection is favoring complexity

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93
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 processGet 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

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94
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

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95
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.. SaltationNOW = we know that saltation is not how it works most of the time – we know it is usally small changes over time

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96
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”

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97
Q

Idea of Inheritance during darwins time

A

Blending inheritance –> - People know that offspring look like parents BUT thought it was a blend of traits - 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

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98
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

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99
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

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100
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

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101
Q

Issue in Mednle’s experiments

A

HE got lucky – the traits that he happened to work with just happened to be discrete traits

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

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102
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

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103
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

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104
Q

Outcome of Modern Synthesis

A

Restated the four postulatesin explicitly gebetic terms
MODERN synthesis = explains evoluton as a fundementally genetic process

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105
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

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106
Q

Postulate #2 After Modern Synthesis

A
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107
Q

Postulate #3 After Modern Synthesis

A

Through differential survival or reproductive sucess not all individuals contibute the same amount to the following generation

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108
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

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109
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

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110
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

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111
Q

Locus

A

Specific location in the genome

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112
Q

Genome

A

Total herediatry information in an organism

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113
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

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114
Q

Gene duplication evens

A

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

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115
Q

Alleles

A

Variant forms of a genetic locus

Example – can have. a C 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)

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116
Q

Polymorphism

A

When there are multiple variants

117
Q

Gamete

A

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

118
Q

Meiosis (overall)

A

Diploid –> Haploid (makes sperm/egg)

119
Q

Mendle’s “Laws”

A
  1. Law of Segregation
  2. Law of independent assortment
120
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
- Each gamete carries one copy into the gamete pool to form zygotes

121
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

122
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

123
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

124
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)

125
Q

When does Independent assortment occur

A
  1. During metaphase 2. During recombination
126
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

127
Q

Deviations from Independent Assortment

A
  1. Linkage
128
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)

129
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)

130
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

131
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

132
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 TWO LOCI genotype ration – 9:3:3:1

133
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

134
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

135
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 likleyP(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

136
Q

AND vs. OR in probabilities

A

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

137
Q

Complication to mendelian genetics

A
  1. Dominance
  2. Epistasis
138
Q

Dominance

A

The phenotypic affects of one allele masks the phenotyopic affect of another allele at the same locus
***It is a type of interaction between allelic varaition at a locus

139
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

140
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

141
Q

Fuel for evolutionary forces

A

Variation

142
Q

Dominanece vs. Epistasis

A

Dominance = interaction within one locus Epistasis = interaction between different loci

143
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

144
Q

Epistasis + Evolution

A

Epistasis is a constraint on evolution

145
Q

Type of interaction in Epistasis

A

Statistical interaction

146
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 effectIf the results = graoh with intersectiong lines then there is an interaction and there is NO additive effect

147
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)

148
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 NSince 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

149
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

150
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 = 22IF 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

151
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)

152
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

153
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

154
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

155
Q

Phenotype

A

The measurable properties of an organism manifested throughout its life
- Any trait that you can measureIncludes: Morphologocal + Phsyicological + biochemical + behavioral

156
Q

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

A
  1. Genetic variation 2. Environmental variation 3. Gene X Envirnment interaction
157
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)

158
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

159
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

160
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

161
Q

What leads to phenotypic plascity

A

Envirnmental varaition

162
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)

163
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

164
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 genotypeIS A statistical interaction – can’t predict the effect of the allele without knowing the envirnment

165
Q

Reaction norm

A

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

166
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

167
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

168
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

169
Q

How do phenotyoically plastic traits evolove

A

By acting on the reaction norm

170
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

171
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)

172
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

173
Q

Genetic Assimiliation

A

The evolution of a fixed trait from phenotypic plastic varaition
***Was an envirnmental trait and is now hardwired

174
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

175
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 traitSINCE – 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

176
Q

Small Scale mutations

A

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

177
Q

Large Scale mutations

A

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

178
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

179
Q

Worse case SNP vs. Worse case Indel

A

Worse Case SNP = change in 1 AAWorse canse Indel = screw up really bad

180
Q

Indels

A

Small inseration and deletions of base pairs - Chnage in length of sequnce

181
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

182
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

183
Q

Gene duplications are due to

A
  1. Unequal crossover (Meiotic error)2. retroposition
184
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

185
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 ***Can cause phenotype – if the longer chromsome stays THEN new offspring might have extra copies of loci = the new loci can have new functions

186
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

187
Q

Chromosomal rearrangements

A
  1. Inversions
  2. Fissions/fussions ***Occur often
188
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

189
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

190
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

191
Q

Importance of Fissions. +Fusions

A

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

192
Q

Fission

A

1 Chromosome –> 2 chromosomes

193
Q

Fussion

A

2 chromosomes –> 1 chrossome

194
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

195
Q

Importance of whole genome duplication

A
  1. May play a role in speciation (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
196
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

197
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 levelIMAGE – shows mutations rates for a single locus

198
Q

Variability in mutation rate

A

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

199
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

200
Q

Consequence of mutations

A

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

201
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

202
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 thebad and fitness bounces back

203
Q

Population Genetics (good definition)

A

The mathematical and empirical study of allelic variationwithin and among populations, including the dynamics of changes in allelic variation through time***All about understanding allele frequcney

204
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)

205
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

206
Q

Why is genotype freqincey not allele frequencey

A

Allle count is NOT the genotype frequincey becasue each genotype has two alelles

207
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

208
Q

Finding allele frequencey from genotype freunecey

A

Freq A = FreqAA + 1/2Freq of Aa Example AA –> 47/147 = 0.314Aa -> 88/147 = 0.599aa –> 12/147 = 0.082Freq A = 0.314 + 1/(0.599) = 0.619
***Don’t divide by anything here because they are already in frequcneies

209
Q

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

A

Equals 1.0

210
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

211
Q

Practice –

A

Freq H+ = 0.8 Freq H- = 0.2Genotype Freq: HH = 0.63Hh = 0.34 hh = 0.03 Freq H+ = Freq of HH + 1/2 Freq of Hh0.63 + 1/2(0.34) = 0.8 Freq of h = 1.0 - 0.8 = 0.2

212
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

213
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)

214
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

215
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 =0.36Aa = 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 generationFreq A = Freq AA + 1/2(Freq of Aa) = 0.36 + 1/2(0.24) = 0.6 Freq A = 0.6Frq a = 0.4Freq 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 aCan call Freq of A “p”; Frequncey of a “q” P + q = 1.0 (Freq of A + Freq of a) = 1.0q = 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 = 0.6P( a sperm) = q = 0.4P(A egg) = p = = 0.6P(a Egg) = q = 0.4P(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 = 0.16NOTICE: 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

216
Q

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

A

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

217
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. recessiveIn an idelaized biallelec system = we can call the frequncey of the other allele “q”

218
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 Pr
obability of getting a gamete with a particular allele is simply equal to the allele frequncey in gamete pool

219
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 poolTHEN – 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

220
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

221
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

222
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 = 2PQFreq 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

223
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 randomViolating 1-4 = changes allele frequncies = generates evolution
224
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

225
Q

Selection

A

Essentially unequal rate. ofsurvival and reproductive success acriss genotypes

226
Q

w

A

Generalized fitness value

227
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)

228
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 = 0.36Aa = 0.48 aa = 0.16 THEN before reproduction a number of mice are eatenAA Survivnng = 288 Aa Surviving. =288aa Suriving = 64OVERALL – 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 uniform2. Need to calulatue NULL – that survival rate is uniform - To find – take total suvivors in population/ total in populations 288 + 288 + 64 = 640 –> 640/1000P(survival) = 0.64 – if it is unifrmTHEN 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 = 307.20.64 X 160 = 102.4NOW have expected survivors 3. Comprare observed vs. Expected survicors AA – 288/230.4 = 1.25 Aa – 288/307.2 = 0.937564/102/4 = 0.625THESE 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 highestfitness genotype to 1 and dividing the others by that value to adjust them accordinglyMke your highest values = 1 and dvide. therest by that value Here : 1.25 is highest –> 1.25/1.25 = 10.9375/1.25 = 0.750.625/1.25 = 0.5 NOW have relative fitness

229
Q

What is needed to quantify survival

A

\Need to compare expected to observed survival

230
Q

Calculating Null for quantofying survival rate

A

Null = that survival rate is uniform Do total amont of surivvors in populations (regardless of genotypes)/Total populations

231
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

232
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 justdepend on these values alone, it depends onthe context of the allelic variation in thepopulation tooNEED 1. Relative fitness 2. Need starting alelelic frequncey

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

233
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/)

234
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 FREQUNCEYdP = 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

235
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 frequenciesA 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

236
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

237
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

238
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)

239
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)

240
Q

Graphs of fitness vs. alelle frequncey

A

Adaptive topograohy
USE the graogs to define an adaptive topography for the popultion

241
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)

242
Q

Fitness differential NS can act one

A

Natural Selection can work on any fitness differential in the absence of other evolutionary forces

243
Q

Rate of change

A

Rate of change is a function of the strength of selection - Weaker selection = takes long STILL IN DIRECTIONAL SELECTION IT WILL END WITH FIXATING FOR HIGHER FITNESS ALLELE

244
Q

When is the rate of chnage the fastest

A

The rate of chnage is the fatstest when the genetic varaition in fitness is highest (P=0.5) - Place where the rate of evolution (rate of alelle frequcney change) is fatstest = in the steepest part of teh curve – always at the same place – alwats when p=0.5 IMAGE – even though all differentc urves (different fitness differential) – the rate of chnage is fasttest when P=0.5

245
Q

Fisher’s Fundamental Theorem of Natural Selection

A

Change in popultion fitness is proportional to varaition in fitness - Fastest rate of chnage in fitness from one generation to the next when variation is highest

  • More varaition = more NS can sort through the variation = fatser evolution
246
Q

Effects of NS

A

NS is determinanistic when acting by itself - If we know the starting point = we can know the end + all of the intermeduary steps - If we know what the conditions are we know what the outcomes will be - NS selection by itself is driven by straight foward mathematics towards a predictable outcome

247
Q

Dominance Vs. recessive in Directional selections

A

The end point is still the same (for domiannet vs. recssive) – still goong to fixation
DIFFERENCE = the rate at which coming to fixation occurs

248
Q

Meaning of S = 0.3

A

Means that 30% difference in fitness across phenotypes Relative fitness = 0.7

249
Q

Selection for benefcial dominant alleles at low frequncey

A

Selection acts quickly but then slows down as the alleles apprach fixation - Selection occurs rapidly because any time the dominant alelle shows up it is seen by Nastural selection = NS can act on it BUT slows down as ut aporaches fixation becayse increase mean popultion fitness to bring it close to 1 = NS can only act on the deletrious recessive allele of which there are very few = Selection slows down

250
Q

Selection for benefical recessive allles at low Frequency (The dominant allele is in high frequncey)

A

Seleection acts slowly but speeds up as the allele appraches fications - NS can only see the allele if it is in aa – if the allele freqeuncey if a is low THEN teh frequncey of aa is even lower because aa is q^2 = have less aa for NS to act on – NS can only act against the A alllele – as frequncey of a increases = maintain varaiance in fitness because of teh heterozygous = NS can accelerate through to end point - NS is slow acting in favor of recssive because recssive won’t have phenotypic affect = NS cam’t fo anything (opposite for dominant because anytime you have dominant NS can act on it)

251
Q

Why is there a difference in change in allele freqeuncey acting against dominent or against recessive

A

The difference is in the average excess –at low frequencies recessive alleles are most likely to combine with dominant gametes –> Therefore, the fitness effect of the allele is invisible to selection because it is mased by the dominant allele - Makes the benefical recessive at low frequencey hace slow chnage but then speed up as the alleles approach fixation Vs. At low frequencies the fitness effect of dominant alleles show up no matter who they combine with however, as they approach fixation, the population mean fitness getscloser and closer to the fitness of the allele –Therefore, the relative benefit of carrying the allele isn’t as strong

252
Q

Directional Selection

A

The highest or lowest value of a trait/alelle frequncey has the highest mean popultion fitness - Will always end up in the same place – fixing for one allele P = 1 OR p=0 = has the highest mean population fitness In the absenece of other forces this leads to fixation for the favored allele

253
Q

When does directional selection apply

A

Only applies if teh relative fitness of Aa is between the bounds or equal to AA and aa - can be the same as AA or aa or in between the values of AA and aa

254
Q

Overdominance

A

Heterozygous advatage – Aa has teh highest fitness

255
Q

Under dominance

A

Heterozygous infiriority – Aa has the lowest fitness

256
Q

Forms of selection

A
  1. Overdominance 2. Underdominance 3. Directional selection
257
Q

Example of Overdomiance

A

Here Aa has the higehst fitness = we set Aa equal to 1

258
Q

s vs. t in selection coefficients

A

s and t keep track of the two selection coeffcinats seeprations
IMAGE A = p –> use s – Selection coefficient acting against A
Aa = t
P –> S
q –> T

259
Q

Example for Underdominance

A

HERE WE MAKE THE LOWEST FITNESS EQUAL TO 1 – divide the absolute fitness by fitness of Aa

260
Q

Selection coeficiants in underdominance

A

s and t are negitive – because the fitness of aa and AA should both be higher than Aa 1 - (-#) = gives a number greater than 1 In under dominencae - scale Aa to one (it will be the lowest – only time you scale the lowest value to 1)

261
Q

When do we set the lowest fitness value to 1

A

ONLY for underdominance (If the Aa has the lowest fitness)

262
Q

What do we calculate for over/under dominance

A

calculate an equilibrium point – static point in system (forces are balanced)
Do this by solving for dP = 0

263
Q

Meaning of Equilbrium point

A

At that point evolution will no longer occur

264
Q

Calculating P> In overdominance Given: s = 0.2 t = 0.1

A

AA = 1-s –> RF = 0.8 aa = 1-t –> RF = 0.9 Aa = 1 – hightest p> = 0.1/().2 + 0.1) = 0.33 - Have equilbirum when p = 0.33 OR when the frequcney of q (a) = 0.67

265
Q

P> in Overdominace vs. nder dominance

A

Might have the same P> value but the nature of p> is difefrent P> for Overdominance is the highest point of fitness P> for underdominance is the lowest point of mean fitness - Fitness is lowest at p> for under dominance

266
Q

Adaptive topography for Overdominance

A

value of P> is the peak – theer is no dP - At the peak there is NO uphill to go = NS will stop (because NS always oushes uphill) - If to the left of the point – then P will increase - If to the right of the point P will decrease - If you start at P> it will stay there –> if you move away from P> it will evolve to go back to P> - The direction depends on alelle frequncey BUT will always fix for the same point - The dP to the left will be posiutive (incvrease P) and dP to the right will be negitive (Push to decrease p)Reason that P> is the highest population fitness in overdomainnece

267
Q

Equillirbium in Overdominance

A

STABLE equillbirum

268
Q

Fixing in Over vs. Underdominance

A

Overdomince = always fixing for one point - No matter the allele frequcney – always fix for the same point Under dominace = there are two points that you can fix for – don’t knwo what wilol be fixed for - What will be fized for depends on allele frequcney

269
Q

Adaptive Topogrphy of Under dominance

A

Still alwats going uphil - if start to the left of p> = the popultrion will evolove to p=0 - If start to the right of P. = NS will push P = 1 - If start at P> and all H-W assumptions are true – it will stary there but only if we keep it there – if it is perturbed = then it wil go uphill in eitehr way depending on how it was perturbed

270
Q

Equillibrium in Under dominance

A

Unstable Equillirbium – does not return when pushed - if you start the poulation on one side it will go to fixation for p = 0 - If you start the population on the other side – it will go to fixation for P = 1Harder to predict end point – depends on the starting allele frequencey - Whether goes to P = 1 or P = 0 depends on the starting allele frequencey (Depends if the starting alelle frequncey starts above or below p>) STILL – both will increase fitness

271
Q

Fitness of Sickle cell in malaria envirnmnets

A

CLEAR case of over dominance AS = the highest fitness AA = get malaria –> S = 0.11 (RF = 0.89) AS = 1.0 – in malaria envirnemnt you are better tan AA because resistant to malariaSS = 0.2 – same in malaria and non-malraia envoirnmemnts – still same fitness decrease as before

272
Q

Calculating the P> + making Adaptive topography for Malaria (With two alleles)

A

Chart = shows that if to the right of equillibriounm in a place with malaria = will increase in S allele (Decrease A) THEN negitive affect of SS is overcome by the increase in fitness oif AS = the frequncey of S will increase until P>

273
Q

Calculating the expected frequncey of Hemolytic Anermia Phenotypes in malarial Envirnments

A

We already know that P = 0.88 –> Q = 0.12 Then we can know the frequncey of indovodulas maintained by NS q^2 = 0.12^2 = 0.014 –> means that 1% of the population is mainatined by NS - If you decrease S NS will push it basck up and increase the number of Individulas that have the disease

274
Q

Result of Heterozygous Advantage

A

The heterozygote advantage of the S allele results in natural selection maintaining a very negative trait – sickle cell anemia- at a rate of nearly 1.5% in those populations!

275
Q

Why Study Evolution

A
  1. Nothing in Biology makes sense except in light of evolution - Consistency in biology = constructions in biology imposed by evolution - No modern biology operates without evolution - Evolution is the process that is repsonsible for biodiversity of the world - Ties together all of modern biology (no aspect of modern biology is isolated from it) - spans all levels of biological organization – links molecules to population’s and ecosystems - It is fundamentally important to much of applied science (Both implicit and Explicit)
276
Q

Evolution leads to

A

Diversity in form + function

277
Q

Evolution + Applied science

A

Evolution = important to much of applied science (Matters in real world) Implicit: Ability to understand systems that rely on evolutionary framework Ex. usefulness of model organisms – need to know ancestry of the organisms - We can then infer our biology based on other animals - Shows why we should be able to learn anything about us from a fruit fly Explicit: Evolution process = part of solution Example – drug resistance (HIV – works on evolutionary concepts and ecosystems) - HIV Antiviral cocktail – works on the evolutionary concept of adaptive landscapes

278
Q

Theory in Scinece Vs. Vernacular

A

Word theory is very different in scienceVernacular: Hunch/speculation/hypothesis Science: Set of overarching mechanisms + principles that explain a major aspect of natural world supported by individual lines of evidence

279
Q

Metaphysical naturalism

A

There is no such thing as the supernatural - means that nothing beyond the physical world exists (the physical world is the entirety of existing)

280
Q

Methodological naturalism

A

Means you can’t rely on supernatural explanations for physical phenomena (for empirical observations) - Need to have this is science (if not then science stops) - Came out of the enlightment – once adopted this idea = then made progress (progress could be made once ascribed to this midset) - Without this we can give up when we encounter something that we don’t understand - In order to science to work = need to operate under unwavering premise of naturalism MEANS – There may be something to exist beyond nature BIT that is entirely outside the bounds of science

281
Q

Root of evolution

A

Evolvere – To unfold + to unroll

282
Q

Biologic Evolution

A

Change in heritable properties of population in organism across generations OR change in allele frequency through time - Population level - Simple definition but plays out in complex ways

283
Q

Implications from evolution

A

Framework of evolutions brought with it some implications –> Challenged some long-held beliefs of the world – changes the way people think about the living world 1. Chnage = the form of the living world - Individual perspective = limited – do not see much change in lifetime – easily in isolation to think that the world has always been the same as the world that you are observing - Accpeted first in geology before biology - Biology was already moving in this direction in the years leading up to Darwin 2. Biologic phenomena are explained by mechanisms concepts - Break from the earlier tradition of Aristotle Final Vs. Efficient causation - Biologic phenomena are not driven by some ultimate purpose 3. History is a crucial part of understanding nature - What we have now results from constraints in history - Historial constrigencey impacts outcomes of natural phenomena4. Variations is ubiqitous component of biological systems - MAJOR break from platonic essentialism –> they thought that variation is just miastakes

284
Q

Broad version of evolutionary biology

A

The study of variation in nature - How variation comes about and how is it maintained and what are the consequences - Looks at lots of time of variation - Looks Within species – Intraspecies - Looks Between species – interspecies - Looks on a phenotypic Level + One the genetic level + ALSO looks at the link between the two - Look at causes and consequences of variation in living systems

285
Q

Stochastic

A

Probabolistic

286
Q

Inter v.s Intra

A

Intra = Within species Inter = Between species

287
Q

Darwin’s mistake

A

Darwin mistake = Endless forms of evolution – not true → more like myriad of forms because have biological contartints

288
Q

Evolution in world

A

Evolution as an on-going process in the natural world.