Co-evolution

Question 1

Co-evolution (long)

Answer 1

“an evolutionary change in a trait of the individuals in one population in response to a trait of the individuals of a second population, followed by an evolutionary response by the second population to the change in the first”

Evolutionary change in 2 populations interacting –> effect each others fitness

Compensatory change in second populations NOT just change in the first – reciprocal evolutionary change – back and forth

Question 2

Co-evolution (short defintion)

Answer 2

Reciprocal evolutionary change across species interactions

Question 3

History of co-eevolution

Answer 3

Importance of species interactions for evolution has been around since the beginning of evolutionary biology
- Darwin = wrote about thinking about evolution in context of community/ecology + complex interactions among organisms
- Dawrin ALSO highlighted the idea of reciprocal evolutionary change – evolutionary process affects species interaction + reciprocal relationship

Question 4

Coevolution Affect

Answer 4

Coeveolution put biotic interaction at the forefront –> placed it at the interface between evolution and ecology
- Thinkning about evolution in the context of ecology + allows ecologists to think about evolution as force in shaping ecology
- Coevolution = represents a crucial link between ecology and evolutionary biology

Question 5

Studying Co evolution

Answer 5

Even though it has been around for a while the framework to study emprically = new + took a while to understand how to study

Question 6

Species interactions in nature

Answer 6

Species interactions are everywhere in natire – effect a wide variety acriss all biological organization

NOT just including oredator orey interactions ALSO explains host pathogens interactions

Ex. pathogen virulence + behaviral manipulation of parasites + geentic varaition in immune systems + insects vectors of plant pathogens + our own mictondria
- All require a co-evolutionary persepctive

Question 7

Species interactions

Answer 7

***Look at the fitness benefit of interaction for both species – Define interaction between species

++ – Mutualism

+0 – Commensalism

+- – Victim/exploitive interaction

00 – Nurutal interaction

-0 – Amensalism

– – competition

Question 8

Mutualism

Answer 8

++ – One has positive on other and visa versa

IMPORANT = needs to be two different species (Cooprotaion is between one species)
- This is two species NOT the same species
- Alturism = same species – similar but same species

Question 9

Species interactions vs. Social behaviors

Answer 9

Species interactions are difefrent than social behaviors in species

Question 10

Commensalism

Answer 10

One benefits – no affect on the other

Example – Barnicle growing on the whale – no decrease in fitness in whale

Question 11

Nuetral interaction

Answer 11

No affect on each other

Question 12

Victim exploits interaction

Answer 12

One species has a negative affect and one species has a positive affect

Victim = species hurt
Exploit = Species benefit

Question 13

Ammensalism

Answer 13

-/0 – Negitive affect on one and nuetral on the other
- If have no affect on one species = no reciprical = NO coevenulation if have ammensalism

Example – Invasive species – ruin native plants = affects others species but no affect on the invasive species

Question 14

Competition

Answer 14

-/- –> 2 species – both negitive affect on each other –> fitness conseqence
- Fitness conseqnece = same as popultion growth – have negitive impact in popultion density

Question 15

What species interactions have co-evolution

Answer 15

++

+-

–

ANYTHING with 0 can’t be because no fitness affect = no change in at least one = no coevolution

Question 16

Parts of Victim exploit relationships

Answer 16

1. Predator Prey
2. Parasitism

Question 17

Predator Prey

Answer 17

Incldudes:
1. Interactions associated
2. Parisatoidism (lay egg in other species = oredator –> NEED to kill = predation)
3. Some herbivory that kills the prey (Things that eat seeds – need to kill victim)

NOTE – In order to get the fitness benefit = need ti kill the victim (exploiter kills)

Example – Boehead whales –> filter feeders == p[redators because kill things

Question 18

Parisitism

Answer 18

Don’t need to kill
- Has many varieties – reap beneift from host that hurt but do not kill

Examples:
1. Most herbavores
2. Pathogenic diseases
3. Brood parasitism –> Mostly birds – lay eggs in other birds species and force the other to raise birds –> Raise babies without adding resource + waste resources on other species
4. Kleptoparaitsim – animals that steal from other animals

Question 19

Range of species interactions

Answer 19

Species interactions can range from diffuse to specialized one to one relationships

Many ways that interactions differ that change the outcome of co-evolution – the degree of specialization affects the outcome

Question 20

Diffuse relationships

Answer 20

No one to one lines = many plants interact with many insects and insencts interact with many plants
- generalized interactions

Question 21

Specialized relationship

Answer 21

Can have very specialized relationship
- Degree of sepcializtion can be one to one

Example – Orchid with long structure for nector with nector at the bottom of the tube = have insect that adapted to polinate this plant – have moth than exclusivley polinates this flower
- Moth only gets nector from this plant and the plant is only polinated by moth
- Very specialized 1:1 relationship

• Example – indiviual relies on other organisms –> endosybiotic – seen in Aphids – need bacteria that grow inside of them –> have bacterua that preforms biochemical functions – need bacteria to synthesize Amino acids – specilaized interaction (living in one organism = 1:1)

Question 22

What type of interaction is coevolution stronger

Answer 22

Co-evolution is a stronger factor in more specialized systems (Not absent from generalized systems but it is harder to study)
- Expect Co-evolution to be string in highly specialized –> if only interact with each other THEN change one one species = affects the other species = co-evolution)

Example – if change in plant structure BUT there are many polinators = won’t affect much because other can take up the space and pollinate

Question 23

Coevolution in more generalized

Answer 23

Co-evolution is NOT absent in generlized interactions BUT not expected to be as strong + Harder to study –> hard to get hypothesis = more studied in specialized

In generalized = has diffrent predictions

Question 24

Co-evolution + Adaptive topographies

Answer 24

Helpful to think about coevolution from the persepctive of adaptive topographies

Overall: As species change on AT they are NOT only chnaging the position of the otehr popultionm on theur AT BUT it is also chnaging the peaks and valleys on the other popultion’s AT
- Chnage selection regime NOT only change position of sepcies – change topography itself

Question 25

Change in AT mindset

Answer 25

Before = thinking of AT As static – species adapted to static set of fiotness conditions –> This assumes that things stay the same from one generation to the next BUT in co-evolution we think about changing AT

NOW = looking at how the AT of one species affects the AT of the other species – In co-evolution At become dynamic

Question 26

Change in AT in co-evolution

Answer 26

Overall: Static –> Dynamic AT

Evolution in one species (movement along their AT) changes the shape of the other species AT
- Peaks change – change because different species change
- As one population changes = optimal genetic combination for other population changes over time

NOW – the fitness peaks change through time in response to change in other popultions – back and forth change = increases complexity in system

Question 27

Quantifying change in Co-evolution

Answer 27

Much more difficult to quantify BUT you can quantify it

Quantifying is an extension of pop gen –> Meshes popultion genetics + ecological interactions

Question 28

Quantifying ecological basis for coevolution

Answer 28

Connection between ecology + adaptation – Lotka Voltera Model of predator prey dynamics

Image:
Chnage in prey density/Chnage in time
- V = rate/density of Prey
- r = rate of reproduction
- P = rate/density of predator
c = capture rate
b = birth rate

Shared parameter = c –> capture rate (how often prey are being killed)
- c = drives the sucess of the prey or predator –> can run through C
- c = function of traits of predator and traits of prey
- What controls the success of predator = function of the trait of predator + function of trait of prey

Prey do good if decrease C
Predator do good if Increase C
- Both optinmize C through own traits BUT optimizng C in opposite directions
- Predator/prey = comes down to rate for C
- evolution = interact with each other in complex manner

Question 29

Capture rate

Answer 29

Evolution of traits that affect capture rate are going to alter the fitness dynamics of the interacting species –> predator prey co-evolution results from evolutionary struggle over C

Question 30

Predation

Answer 30

An ecologic interaction in which one species kills and consumes another
- Prey = necessarily killed
- Includes Predator prey + Parasistoid

NOT including parasites

Question 31

Predation in nature

Answer 31

Predation is ubiquitous in nature – across all ecosystems
- Organisms are heterotrophs that kill other organisms

Predator prey = easy to understand

Question 32

Defensive traits in nature

Answer 32

Defensive traits are ubiquitous in nature – also everywhere
- Defense to predation through behavioral traits + venom + stings + running fast

MEANS – have predation everywhere + have many defensive traits –> might be result of co-evolution

Question 33

Traits involoved in predation under selection

Answer 33

Look at selection affecting defensive traits

Example –> looking at lizards with hrons + birds (predators)
- Purching birds – have no talens = to kill prey they impale it on spike in tree (put prey on spike)
- reserachers measured horns on lizards to see defensive traits and see which lizards were killed by birds – looked at horns of killed liozards vs. horns in overall popultion of lizards to see if have selection on defensive traits

Results: Lizards killed have smaller horns = have different trait values = trait is under NS

Question 34

Is bird example co-evolution

Answer 34

Have evolution of one species (evolution in lizards) BUT need reciprical evolution to be co-evolution (Evolutionary response to evolution in another popultion)
- Here we have adaptation in one direction but do not expect chnage in birds because the birds can eat other things –> Therefore the chnage in lizards to be more defensice = does not have a big influence on the fitness of birds = birds won’t change

Question 35

Example of Co-evolutionary Arms race

Answer 35

Rough Skinned newts – reciprocity is investigated

Backgroun – had a case of 3 people in Orgean that all died – tehy found newts in coffee pot
- Looked ot see if the newts were toxic –> grind newts and put in mice –> Small amount of new killed many mice = toxic –> has a lot of nuerotoxin

Why have toxin on skin –> Found garner snakes who had eaten newts – shows some snakes can eat them and sepcialize to eat them –> snakes adapted to eat organisms

Snakes have chnage in Amino Acid in sodium channel that prevents TTX binding = can’t hurt them
- Molecular adaptation in predator + Adapatation in toxicity in newt –> coevolutionary arms race between species

Question 36

Toxin in Newt Example

Answer 36

Toxin itself = people didn’t think that organsims should be able to evolove defenses to it

Toxin = Tetrodotoxin (TTX) –> Dangerous because nuerotoxin –> Binds to all vertabres – attatches to voltage gate sodium chanel on nervous system
- Toxin shuts them down = attaches important part of nervous system – conserved part of nervous system

Question 37

If resistent alelles that allow snakes to eat newts cause more resistence in some but less resistnt in other –> why have variation (Why not fixed for most resistent)

Answer 37

Question = why not just fully resistant sweep through population

Answer: There is a strong fitness tradeoff
- making sodium channels resistent to TTX binding also makes them bad at being sodium chanels

If can eat newts when available it is good to have resistence when can BUT have strong fitness tradeoff
- Snakes with resistnace have a less efficent nerous system (clumpsy + slow)
- Newts are slow = resistent can be resistent but they are more vulnerable to other predators

Reason = Antagonist pleotropy

Question 38

Why have fitness tradeoff in newts

Answer 38

Antagonist pleotropy – Alleles on sodium chanel = affects different traits

INcrease resistence to TTX but decrease speed of nervous system

Question 39

Which way will newts evolove

Answer 39

Which way they evolove = depends on the ecological envirnment

Different in predator or different if in high newt envirnment –> plays out in complex ways

How the tradeoff is resolved (what is the optimal balance between next toxin susceptibility and speed) comes down to the overall ecological context of the interaction

Question 40

Coevolution varies strongly with…

Answer 40

SPACE – co-evolution relationship varies stringer across space

Question 41

Co-evolution + Space

Answer 41

Co-evolution relationship varies stringer across space

regions where newts are highly toxic = overlaps in regions where have high resistent snakes
- Matched by variation in predators + varaition in resistence

Leads to hotbeds correspinding to process across space

SHOWS – that looking in difefrent subdivided popultions = gives window into process

Question 42

Basis of empircal framework for co-evolution

Answer 42

Geographic change in evological structures = basis of empircal framework to study

Because – looking at subdivided popultions gives us a window into process

Question 43

Spatial varaition + Co-evolution

Answer 43

Co-evolution interactions vary strongly across space – spatial varaition is crucial for understanding process of co-evolution
- If co-evolution is occuring –> can we make inferences about chnage from one popultion

Hard to study co-evolution –> We are limiting to tracking evolution through time – hard to track through time

Question 44

Limiting factor in co-evolution

Answer 44

Time is a limiting factor for studying co-evolution –> the reciprical dynamic nature of co-evolution plays out over many generations
- Hard to study co-evolution –> We are limiting to tracking evolution through time – hard to track through time

Question we ask in studying = Is reciprical evolution taking place in popultion?

Question 45

Difficulty in studying Coevolution example

Answer 45

Example – Parsnips –> defended from insects by producing a compund with with smell BUT have insects that specialize in eating parsnip leaves
- Parsnips = have furanocoumarins in leaves –> the compund goes ebtween DNA to cause cell death
- Most insects can’t eat the leaves but have a worm that can attack because has high Cyt p450 detoxification

Reserachers = go to feild and look at parsnips (look at furan levels) + look at worms (look at Cyt p450 levels)
- Might see both are high and both are low

What does this tell us – expect that this is a back and forth process but we do not know where in process we are looking
- over time we might see shift in fitness of organisms (parsnip increases and warm decreased – as warm increased then parsnip decreases then parsnip increases and worm decreases thne have chnage in worm again)
- we expect this to play out across genertions but when looking at one time point in generation you might have high fitness in parsnip and low in warmn BUT this tells you nothing about co-evolution process

Question 46

What does observation in co-evolution process tell us

Answer 46

If we study a particular population and find very high
furanocoumarin levels in the parsnip and highly upregulated P450 in the caterpillars, what does that tell us?

Answer: We expect this to play out across genertions but when looking at one time point in generation you might have high fitness in parsnip and low in warmn BUT this tells you nothing about co-evolution process

Question 47

Studying Co-evolution in broader patterns across species

Answer 47

Looking across more species

Example – Looking at pigeons + bird lice –> look at traits of birds + traits of lice –> does this tell us about co-evolution driving intercation

Answer: NO - can have traits that match but doesn’t tell us if traits evolove due to co-evolutionary response
- Could be that lice happen to have structure ro attack birds
- Doesn’t tell us if driven by co-evolutionary process

SHOWS – hard to know if driven by co-evolution

Question 48

Fixed differences among species

Answer 48

Fixed differences among species make it hard to generate testable hypotheses about the dynamic nature of coevolution – hard to say if something is driven by co-evolution

Question 49

How to test co-evolution

Answer 49

Can generate testable hypothesis if look at varaition in between the hypotehsis of adpation within popultins and fixed differences among species (variation in middle of these allows us to construct better hypothesis about dynamics of co-evolution) – varaition across subdivided popultions in difefrent ecological envirbnments tells us about hypothesis to study

Previous hypthesis about co-evolution focused on adapation withon popultions or fixed differences among species –> focus on these hindered development of framework to study co-evolution

Question 50

Geographic mosaic theory predictions

Answer 50

1. Interspecific interactions vary across populations
   
   • Co-evolution varies across popultion
   • Have lots of varaition (like variation in degree of sepcialization in popultion)
2. Coevolution of species interactions will also vary among populations
3. Populations differ in their degree of specialization
4. Differences in the outcome of species interactions and
   specialization in different ecological contexts scale up to a form a geographic mosaic of evolving ineractions

Question 51

Geographic mosaic theory (overall)

Answer 51

Used to study co-evolution

Question 52

Geographic mosaic theory (overall)

Answer 52

Used to study co-evolution – context of how co-evolution is studied

Question 53

What is included in ecological conditions

Answer 53

Biotic + Abiotic

Question 54

Why mosaic in mosaic theory

Answer 54

For moasic – look at any one tile and doesn’t say anything but look at all popultion and tells you more about overall dynamics of system

Key to the picture = differences among popultions viewed from a higher perspective

Question 55

Using Geographic mosic theory in Newts + Snakes example

Answer 55

We see “hot spots” and “cold spots” in the arms races
In some populations the players are equally matched, when this snake/newt interaction is at the forefront of fitness for both populations

In other ecological contexts – other factors are more important for driving population dynamics so the arm’s race isn’t as strong

Question 56

Parasites vs. Predator prey

Answer 56

In predation/Prey – We are looking at something that was always a life or death situation – predators are evolving more effeicnetely to capture and kill prey while prey are evolving to espcape cature or defened themsleves –> It is inheritley an arms race situation
- No other way to go –> constant antagonsim

Similar arms race with parasites – parasites are evoloving to take better advantage of the host’s resources while the host is evolvong to defend itself against the parasite BUT there are other options on the table

Question 57

Arms Race in Parasirsitsm

Answer 57

Might have an arms race BUT not needing to be killed (like in predation) opens up other ways to play out

Way adaptations affect traits that make routes of coevolution more diverse

Question 58

Evolution in parasitsim

Answer 58

Instead of escalating antagonism parasites can evolove to get along with their hosts

Result: Complexity of parasite lifecycle can result in tradeoffs between different component of fitness – Dynamics can form tradeoff in parasite

Question 59

Tradeoff in parasitsim

Answer 59

Fitness of parasite’s growth and reproduction with host Vs. Fitness of parasites ability to be transmitted between hosts

For parasites to be successful they need to leave to another host – creates tension where have within host vs. between host dynamics
- Tradeoff in different part of lifecycle is important

Question 60

Tradeoff in parasitism Process

Answer 60

If a parasite is able to use more of the host’s resources it will have a growth and reproduction advantage within the host BUT making the host too sick or killing it too quickly can negitivley affect the parasite’s chances of passing offspring to anew host making the current host a dead end
- Genotypes that are successful in exploiting host = might be most successful within the host BUT the genotype can be a dead end where it is good at reproducing within the host BUT might kill host before offspring go to another host

Example – Within the host –> The most virulent strain might win out within the host

Question 61

What wins in between vs. within host in parasitism

Answer 61

Between host transition outweighs the within host adapataions because it is critical trait

Fitness = 0 IF can’t go to a new host

Question 62

What drives within vs. between

Answer 62

Antagonist Pleitropy drives within vs. between in adaptation
- Most adaptations = driven towards getting out of host and into another

Question 63

High fitness in host

Answer 63

High fitness in host drives the host to be in bad shape that limits the offsrping going to a new host –> kill host before transmit offspring to other host = evolutionary dead end

***Shows fitness within vs. Fitness between

Question 64

Patterns due to within vs. Between

Answer 64

1. Selection on parasites to infliuence the phenotypes of the host in way that increases tranmission –> Extended phenotypes
   
   • The phenotypic effect in other organisms can cause selection to act on the allele frequencies of the carrier organism
   • Many examples in nature –> many where the parasite affects the physiology or behavior of the host

Question 65

Extended Phenotypes

Answer 65

The phenotype affects of a gene aren’t limited only to the organism that carries the gene
- Effect of alleles extends beyond the organism that contains the allele

The phenotypic effect in other organisms can cause selection to act on the allele frequencies of the carrier organism

Example - Gall size – extended phenotype of insect

Question 66

Manipulation of Host behavior and physiology Examples

Answer 66

1. Gyardia –> Gives you symptoms that are to get you to put the bacteria back into the water supply = extended phenotype of organism
2. guinea worm –> Larvae stage gets to the legs –> very painful –> only thing to make it feel better is to put leg in water –> the warm leaves the leg to go back to water to get eggs in water
3. Cortifects –> behaviral manipulation of host
   • Fungues grows in brain of ant –> makes ant leave the colony –> goes to branch and bites onto leave –> eventually spur grows out of ants brain and goes to ant mass
   • Maximize transmision of parasite into nest

***Humans are suceptible to behavrial manipulation of parasites

Question 67

Option for parasite transmission

Answer 67

Opption 2 = complex lifecycles involving vectors –> to go between hosts and to get resource from host
- Can be complicate life cycle with many hosts + multiple vectors

Example – Vector mediated disease
- Malaria – maquitoes are the vector (intermediary host)
- Chargas – Vector by kissing bugs –> insect takes blood and lays egg in host –> when bite they defecate where they feed – bite itches = rub the feces into the cut = Parasite gets into body = disease

Question 68

Vectors

Answer 68

Intermediate hosts involved in parasite transmission
- Intermediate system

Question 69

How to control vector mediated disease

Answer 69

Contol parasite by controling vector insect

Question 70

3rd option for Parsitism within vs. between

Answer 70

Attenutaion of virulence –> parasites can evolove exploitative restraint if it maximizes between host tramission
- Parasite can evolve to get along with the host to increase chance if going to other organism
- restraint in exploitation = the host stays healthy = parasite can get to other host

By becoming less virulent they can weaken the fitness consequneces for the host – weakens the selection pressure for defenses

Question 71

Effect of attenuation of virulence

Answer 71

If parasite starts relaxing fitness affect on host -= decrease pressure of host resistence on parasite = host will not develope resources to fight pathogen = can evlove to tileratre –> NOW go from severe disease to having some fitness consequence but not major
- Tradeoff you can expect in an emerging disease

Question 72

Example of Attentuation of virulence

Answer 72

Rabits + Myxoma

Rabits - were a big problem in Australia – popultion exploded –> many attemptes to control rabits
- Had European rabits (European rabits in America got very sick rom Myxoma virus – leads to rapid tumor growth in rabits –> kills rabit)

Idea = use pathogens (parasites) for control pruposes –> get leath diease and infect rabits in australia –> should sweep through and get rid of disease

Start = infected 100 rabits –> inject with virus – IT WORKED well at first (50,000 –> 50 rabits)
- All rabits left had not been infected – no rabits infected live (lethality = 99.9%)
- Population of rabits decrease

Rabit popultion became much less dense and the limiting factor for virus became transmission
BUT THEN rather than going to exictiction –> effect leveled out quickly
- At 25% of popultion = NOW rabits are less dense = limiting fcator is hosts ability to infect others – as popultion decreases the probability of infecting others decrease

END = have chnage in selective pressure on virus

Question 73

What happened to virus in rabit popultions

Answer 73

Rather than going to exictiction –> effect leveled out quickly
- At 25% of popultion = NOW rabits are less dense = ability of virus killing host completley = limits fcator of hosts ability to infect others – as popultion decreases the probability of infecting others decrease

END = have chnage in selective pressure on virus

Over time virulent strain decreases in popultion – Changes so that the strain that is most common = when rabits live longer
- Highly virulent virus becomes extict and most starins only kill 50% of the time but rabits loive longer –> rabits now have time to get other rabits sick

Question 74

Where is shift in lethality (parasite or host resistance)

Answer 74

Shift occurs on parasite side

In example – rabbits are somewhat more resistent BUT this is small affect + not at all of the virus had’t chnaged first
- Easy to prove with experiment

***If virus didn’t change the rabits would be extict

Question 75

Australia rabits now

Answer 75

Austalia = Still have rabits + Myxoma BUT they are at a stalemate because of attenuation –> can’t transmit = favor phenotype that case the host to be less sick to be able to be transmitted

Question 76

Vector host + fitness tradeoff

Answer 76

Vector hosts do not have to worry about fitness tradeoff –> as long at the vector is alive doesn’t matter how sick the host is

Question 77

Effect of less dense host popultion

Answer 77

Less dense host popultion should lead to rapid attenuation in parasite

Question 78

Rabits (Slides)

Answer 78

The strain of Myxoma introduced had >99% mortality and no infected
rabbits lived more than 13 days

Within 2 years, the population dropped by more than 75%

Rabbit populations become much less dense – and the limiting factor for virus fitness became transmission

This led to the rapid evolution of less virulent strains –allowing rabbits to live longer, and be more
likely to transmit the virus to new hosts in the new, sparser populations

The control effect of Myxoma
leveled off, and in 5 years, the highly virulent strain was almost non-existent

Question 79

General dynamic expected in emerging pathogens

Answer 79

Atenutation of virulence indicative of general dynamics we expect with emerging pathogens
- If host decreases = have different pressure on parasite where expect that they will get along better with host

Process – pathogens evloving to survive grow and spread in a new popultions

In the long term attenuation of virulence is a likely outcome but we can’t relay on that in human epidemics

Question 80

Apply Attenuation to human epidemics

Answer 80

Issue = can’t bank on human pathogens without massive mortality = need decrease in host BUT we have norms to force through our own actions

To decrease without people dying = can limit contact during time of emerging pathogens

Example - Omicron = less suck but more transmissible –> happened without people dying but with policy to limit transmitability

Question 81

Emergence

Answer 81

Something we pay attention to now – how we model

Epidelogical models come from co-evolutionary models of host parasite

Question 82

Probability of emergence

Answer 82

Determined by reproductive ratio (R0)

R0 = BN/Gamma + alpha + delta

N = size of host popultion
B = transmission rate to suceptibe hosts
alpha = mortability due to infection
Delta = natural host mortality rate
gamma = rate of recovery from infection

Question 83

R0

Answer 83

Expected numver of secondary carriers from each primary case of infection –> how many other people will be infected by that first infection

Question 84

R0 Values

Answer 84

R0 > 1 = can cause epidemuc –> can grow effectivley

R0 < 1 = pathogen requires adapation first before foothold in popultion – can’t cause an epidemic
- Many bad diease <1

Example - MERS = <1 –> only get from cammals (no human to humans)

Question 85

What drives R0

Answer 85

Reproductive ratio = function of transmission rate (B) of parasite to host multipled by the size of the host popultion (rate of getting transmission) THEN deivided by naturalo mortality of host + death due to infection + recivery from infection

Can increase R0 by increase B or decreasing alpga or gamma
- Traits can be under selection to drive emerging and increase tramsnisaboloty but decrease mortality and decrease ability to recover (less sick but more sick for longer) –>THIS is the evolution we expect for Adapative topographies of pathogens through time

Question 86

Expected evolution on AT for pathogens over time

Answer 86

Decrease mortality and decrease ability to recover (less sick but more sick for longer) –

Question 87

R0 is…

Answer 87

Context dependent (NOT for pathogen as a whole)
- Host affects transmissability + rate of recovery –> R0 is NOT fixed parameter for pathogen

Question 88

Humans + R0

Answer 88

Humans can directley manipulate many of the factors driving R0
- try to dirve Ro down by limiting transmisability + limiting host density (policy came out of parameter for understadning co-evolution of pathogens)

Question 89

Vaccine + co-evolution

Answer 89

Look at coverage of vaccine to see when will viryu change to reimerge to epidemic levels

Question 90

Our desions are…

Answer 90

Extended phenotype of virus –> when had less deadly (sick but less dyring) we stopped health measured when didn’t help as much

This invcreased the transmisability because less distanced = policy to increase or decrease distancing is based on the genotype of the virus = extended phenotype of the virus on us as host

Question 91

What does the evolution of reduce vriulence show

Answer 91

Shoes that antagonist interactions exist on a continium

Question 92

Continum of antagonist interactions

Answer 92

We can see examples of decrease in fitness determinetal of parasite to host –> continium of lethal to enetriley neurtal (commensalism) BUT the continum does not stop at zero instead it goes from nuetral to benefical interactons
- See parasites + mutalists on continum with each other BUT they are connected

Example – In Myxoma see shift from lethalioty to less degree of lethality

Question 93

Parasitses + mutatlism

Answer 93

Parasitism + mutalism exist on the same continuum–> if can go from lethal to moderate thne can go (evolove) from anatagonist to cooperative relationship

There is pressure of to be less lethal over time AND for mutalism an organism could give resources but if cheat benefit then evlove towards lethal towards parasitic relationship = co-evolutuionary frameowrk predicts that many specialized interactions exist in the middle ambigous zone between parasite and mutalist

Question 94

Where are most intearctions going to fall

Answer 94

Co-evolutuionary frameowrk predicts that many specialized interactions exist in the middle ambigous zone between parasite and mutalist
- Place in middle = expect place to occupy in long term

Question 95

Example Shift from pathogen to mutalism

Answer 95

Joen was studting cyto-nuclear stabilty using Ameobae (removed nuclei to understand function of cell compnents) – THEN some of his labs strains became infected with a parasitic bacteriam

Intially almost all of the ameoba died and those than survived showed decreased growth and fitness

Jeon nursed the infected strains for 5 years and the infection persisted BUT the ameoba got better (fitness recovered)
- Ameoba increased fitness even though still infected
- Before had a big die off then those thats tick around have less health issues = meybe ameoba increased resistance or had less virulent bacteria BUT it is not attenuation

BUT this was NOT just the case of attenuated virulanece

Question 96

What happened after 5 years after Ameiba were infected

Answer 96

After 5 years survivorship shifts = increase growth rate – still infected but to lower extent

NOW = have strain of ameoba that are infected with lower fitness AND have initial uninfected lines

Exp – swaped nuclei (move genetic material) to other –> swap nuclei between infected and not infected + did the same in infected
- Infected –> unifected = fitness decreases
- Swap infected for non-oingfected = 93% Survival rate (infected nuclues in no bacteria presnet cell = 6.6% SR)

Found: Bacteria are obligate oarasites of the ameba – had genetic change in ameoba to coorportaion with parasite

End = have highly deleterious pathogen to a situation where bacteria is depended on host but host is dependent on bacteria –> evlove to cooporate and utilize the pathogen (get parasitsm –> oblogate cooperation)

Question 97

Mualitsic endosymbiosis in nature

Answer 97

Mutalistic endosymbiosis are very common in nature – many may have evolved out of parasitic relationships
- Commonality of symbiosis in nature suggests that they are more common than we think
- Have long term relationship where organsisms live in cells of others

Question 98

Examples of endozymbiosis in nature

Answer 98

1. Aphids – bacteria to be able to eat plant cell
   
   • Intracellular + vertically transmitted + start life living with bacteria in cells
2. Mixoctricha paradox –> lived in termites to digest cellulose
   
   • Mixonctricha by itself is build of endocymbiotyic interactions –> Not just one organism (have bacteria on outside of it that function as cillia – involoved in motility of organisms through termite + have bacteria inside that could function instead of mitocondria)

Question 99

Vertically Transmitted

Answer 99

Mother –> offspring

Question 100

Two organelles that are result of endosymbiotic origin

Answer 100

1. Chloroplasts –> look like cyanobacteria
2. Mitcondria –> Look like plha proteobacterium

***Thought to be derived from endosymbiosis – derived from bacteria that have symbiotic relationships with Eukroyotes

Question 101

Initial similarity in mitocondria + chloroplasts

Answer 101

Initial similarity = from microscope but then took seriously when saw mitocondria have their own genome that look like prokayotic genome –> Shows result of long term endosymbiotic relationship

Question 102

Genes in mitcondria

Answer 102

In animals – only 35 functional genes (with very
few exceptions) all occurring in the same order
- genome is highly conserved –> high specilization of genome = strong pressure to stay this way

Most genes functioning in mitochondrial processes now reside in the host genome – but they are of mitochondrial origin
- Don’t just use 35 genes – most genes are needed for job are now houses in host genome – prokyotic genes but in nucelar genome = shift of mitocondria genes in nuclear genome = hroizontal gene transfer

Question 103

Shift of mitocondrial genes

Answer 103

Don’t just use 35 genes – most genes are needed for job are now houses in host genome – prokyotic genes but in nucelar genome = shift of mitocondria genes in nuclear genome = hroizontal gene transfer

Mitcondrial genome –> host genome – Get some exchange of genes across phylogenetic branches

Question 104

Horizontal gene transfer

Answer 104

Movement of heritable genetic material among individuals other than parent-offspring relationships
- Exchange of variation within species BUT across unrelated indiviuals

***In many cases this is across species barriers

***Mitcondria transfer = one of most important

Question 105

Easy of mitocondrial gene transfer

Answer 105

Hard to do:
- Need whole coding region (inract coding region has to be inserted)
- Inserted into place where would cause problems
- Needs to be inserted in a way that it will be transvcribed +_regulated
- Have big difference in geentic code (mitcondria have different code) = need to change to match code

Question 106

How did horizontal gene transfer happen sucessfully

Answer 106

Happened a lot of time but wasn’t always successful –> lots of random shift won’t fulfill the requirments BUT when it does NS can act fast to keep it conserved across all animal life

Question 107

Why favor Mitochondria gene transfer so strongly

Answer 107

Most genes in nuclear genome = mitondiria as independent organisms seed control to lifecyle of hist –> prevents mitocndria from backslideing on continium – can’t evolove indenentley = can’t backslide
- Otherwise mutatios in mitocodnria in cells that is independent for growth + reprdouction – we can expect it to cheat and stop giving cells –> prevented by horizontal gene transfer

Question 108

Mitocondria endosymbiosis (overall)

Answer 108

2 organisms fusing to be one that NS acts on as a whole

Got mitocondria from long term mutualistic relationship with bacteria