Is the change in form/behaviour/DNA of an organism over time.

our Def: Change in allele frequencies in a population.

caused by:

1)natural selection

2)mutation

3)migration

4)genetic drift

Phylogeny shows relationship

-the tips of tree are extant species

-the nodes are common ancestors

-sister taxa: closest relative from common ancestor

-when using form, get different trees depending on which trait is used (spots, hair color, etc)

*build trees /w multiple characters!

*always use homologous characters!( ie. not wings of bats/birds)

-simliar feature due to descent from common ancestor (ie. forearm of mammals)

analogy: (convergent evolution) - similarity due to selection presure or enviornment (ie wings, shapes of sharks/dolphins)

molecular homology: "universal code" - amino acid formation

-processed pseudogenes (nonfunctional copy of a gene) lack promoters and introns, and can be used to estimate age, as well as when a common ancestor was shared.

-pseudogenes occur when gene goes from DNA to RNA and back to DNA (reincorporated)

-when RNA is process, introns removed and polyA tail is added, and therefore when it becomes DNA again it does not have a promoter or introns (useless)

Lamarack (1809) - argued that species change into new species

-argued that acquired traits were inherited

-this is not true... don't inherit muscles, dyed hair, etc

Mendel- work was lost temporarily

Wallace and Darwin

-evolution (descent with modification) and natural selection

-evolution is not progressive (newer not better)

-evolution is not 1-dimensional

1. South American fossils resembled living animals

2. Parts of the world with similar climates (ie. Aus+S.Am) populated by very different organisms (ie. polar regions... polar bears and penguins)

3.Plants and animals on each continent are distinctive (why are marsupials so abundant in australia?)

4.Many specis on oceanic islands are found only there (endemic) (Galapagos finches)

5.Endemic species on islands closely resemble species on adjacent mainland (likely colonization + similar ancestor)

woodpecker finch uses a stick in a hole to acquire grubs

-combined natural selection with Mendelian inheritance

population genetics: how one species becomes two

-this was in the 1930s... DNA discovered in 50s

Organisms are adapted to their enviornment by natural selection.

Woodpecker adaptations:

-thick skull

-strong beak

-specialized claws (grip)

-prey detection

-camo (light belly/dark back)

-neck muscles

-tail feathers

-short legs

-long tongue

natural selection: some individuals in a population produce more offspring than others (ie. are more fit)

-not always slow (ie. HIV)

ORIGIN

-65 million infected

-1/3 died

-uses macrophages and T cells to replicate

HIV1 most closely related to chimps

HIV2 to other monkeys

the VIRON

-diploid ssRNA genome

-surface proteins

-enzymes:

---reverse transcriptase (RNA to DNA)

---integrase (splice HIV DNA into host)

---protease (process HIV proteins)

-host has CD4 and co-receptor

HIV1

-three separate transfers (groups M,N,O)

-humans and chimps have 98% similar DNA, but only 2% divergence

-WITHIN subgroup M there is 20% divergence, and there is 35% divergence between subgroups M,N,O

-this is huge

AZT - a drug used early on

-replaces OH on DNA with N3

-stops reverse transcription (can't' add nucleotide)

-over time, AZT becomes ineffective

-virus adapts... resistence in patience to AZT increases over time

-they think that AZT is being stopped from being incorporated

CCR5

-co receptor

-mutant allele (delta32)

---32bp deletion

---resistant to HIV (HIV can't enter cell)

---9% Europeans contain allele...absent in Asians and Africans

---more frequent in N Europe due to selection and drift (gene was useful during Black Plague)

WHY CAN HIV MUTATE SO QUICKLY?

-generation time

-single stranded RNA- no fixing or proof reading

-surface proteins - selection

-population size

allele: sequence variant (version of a gene)

locus (loci pl.): position on chromosome, MAY correspond to a gene

-can have several alleles at a locus (usually 2 for us)

allele frequency: proportion of specific allele in population (frequency A = # copies of A/2N (for diploid-2N-species)

genotype frequency: proportion of individuals with specific genotype

-proposed by Darwin and Wallace in 1858

"process by which biological populations are altered over time, as a result of the propagation of heritable traits that affect the capacity of individual organisms to survive and reproduce"

REQUIRES:

-variation

-heritable trait

-differential fitness (ability to survive and reproduce)

-reproduction

Other mechanisms of evolution include genetic drift, gene flow, and mutation.

TWO TYPES:

-ecological selection (predators, food)

-sexual selection (competition for mates)

-like natural selection, but humans select traits

-flower development...

CAULIFLOWER gene

-254 aa long, and binds to DNA to activate other genes

-multiple alleles

APETALA1 gene

-functionally similar to CAULIFLOWER

-cauliflower, broccoli, burssel sprouts, kale, kahlrabi, cabbage are all from same species

-species has both CAULIFLOWER and APETALA1

-many different flower results depending on whether these are normal or mutant

-in cauliflower plant, found that at a.a. 151, GAG was TAG (mutation that created stop codon)

-one nucleotide substitution, and therefore premature termination

-in wild cabbage, 2/11 alleles had premature termination

-in kale, 3/7

-in brocoli, 8/9

-in cauliflower, 10/10

**domestication selected for mutant CAULIFLOWER allele

Can natural selection by bumblebees cause evolution of a floral trait?

-experiment.... used 48 plants

-single color gene (2 alleles)

S_ = yellow dot flower

ss = all yellow (recessive)

-started with 25% ss and 75% S_ (1:2:1)

-all plants survived

-plants with yellow dot had more seeds and was visited by more bees

-changed allelic frequencies... increased 's'

*therefore, bumblebees can cause evolution of floral trait

***********

NATURAL SELECTION ACTS ON INDIVIDUALS, BUT AFFECTS POPULATIONS

******

NATURAL SELECTION ACTS ON PHENOTYPE, BUT AFFECTS ALLELE FREQUENCIES

***********

in selection, individual DOES NOT CHANGE~!!

DIRECTIONAL SELECTION

-original population distribution of a heritable trait shifts along a continuum.

-ie... medium ground finch beak depth increasing during dry years, and decreasing again afterwards

DIVERSIFYING SELECTION

-ie. hybrid inferiority

-black-bellied seedcrackers... NOT sexual dimorphism (can still interbreed)

-lower bill width concentrated at certain areas (ie. 13 mm and 15 mm, but not in between)

STABILIZING SELECTION

-making population less diverse along continuum

-ie. infant birthweight (can't be too small or too big)

-hybrid strength!

1)historical constraints: new species originate from existing species

2)adaptations are compromises: single structure often has multiple functions

3)evolution is not only the result of adaptation: some of it is due to chance (genetic drift, mutation)

4)acts on existing variation: does not create new alleles (unless mutation)

-morphological

-biochemical (proteins (ie. Drosophila Adh - alcohol dehydrogenase))

-DNA (also affects proteins, but more variation)

-cellular (number of chromosomes, gene order(inversions))

Grasshopper has two chromosomes (CD and EF)

-each can be standard or inverted

-can look at fatalities, viability, and weight of different combinations)

DIFFERENTIAL REPRODUCTIVE SUCCESS

-sparrowhawks.... 72% females die before sex mature (ie. only reproduce less than max)

-those who make it have huge numbers of offspring)

Purines: adenine and guanine

Pyrimidines: cytosine and thymine

-these are nitrogenous bases

-DNA also consists of a phosphate group and a 5-carbon sugar

-DNA molecule has sugar-phosphate-sugar-phosphate backbone

transition: (ts) purine purine or pyrimidine pyrimidine (A<>G or C<>T)

transversion: (tv) purine pyrimidine (A<>C or G<>T)

-transitions more common, due to size of nitrogenous base (ie. single or double ring)

-single nucleotide

-may create new allele

-caused by random error during either DNA synthesis or repair

If mutation is in coding region:

-replacement/non-synonymous (a.a. substitution)

-silent/synonymous (no a.a substitution)

-can have base-pair substitution (no effect on a.a sequence, missence, or nonsense)

nonsense = insertion of stop codon

missense= difference a.a.

-can have base pair insertion or deletion (frameshift cause extensive missense, frameshift cause immediate nonsense, insertion or delection of 3 nucleotides ields no frameshift)

-typically far more synonymous nucleotide substitutions occur than non-synonymous

transposons

read about this?

-problem with terminology...

-not all mutations result in loss of function

-not all mutations occur in coding regions

-regulatory proteins can turn on functions (ie. suppressors)

High mutation rates can be advantageous (new habitat, unstable environment)

-most mutations are not deleterious

-when new mutation occurs, selection may act

selection coefficient: fitness difference control vs experiment

-in e.coli, greater than 70% of mutations have selection coefficient of less than 2% (selection acts but is very small)

Gene duplication

-unequal crossing over (prophase meiosis 1)

-crossing over can lead to two genes on one chromosome

-only need 1 copy to remain functional, other can do something else

duplicated genes

-structurally similar

-similar function

-clustered on same chromosome if result of inversion

-occasional pseudogene

-ie. gene for ribosomal RNA (need lots)

paralogous: similarity due to duplication (parallel line not common ancestor... result of duplication) (a1 + B1)

orthologous: similarity due to ancestry (B1 + B2)

(new genes and duplication example)

Ancestral globin gne was duplicated, then mutated in both copies (to make different)

They were then transpositioned to different chromosomes

Further mutations and duplications then occurred

Alpha, beta, and epsilon globins are fairly similar still

-differ in cap site, exon length, size of amino acid, intron length, and polyA site/length

***still similar sequences and domains

-there are now many different globin genes, within alpha and beta families

-myoglobin is a pseudogene and can be traced back 600-800 million years ago

-alpha and beta families split off around 500mya

-fetal hemaglobin... just before birth there is a switch from y-globin to B-globin expression due to oxygen affinity (thus commences the creation of more bone marrow)

INVERSION

-Drosophila...

-Old World spp. have cline (change in freq /w lat) with series of inversions (due to adaptation?)

New World... Chile 1978 and Washington 1982 both had same set of 19 inversions...

-similar clines in both new populations

-same as Old World

-What genes are found in the inversions???

-inbreeding exps allowed to see homozygous form

-affects body size (small body for hot dry areas and large body for wet cooler areas)

POLYPLOIDY

-extra copies of entire chromosomes

-common in plants

-rare in animals (earthworms can self fertilize, some asexual animals such as goldfish, moths, salamanders)

-can lead to instant speciation

Plant parent...

-mutation causes production of diploid gametes... causes 4n from 2n gametes in first generation

-can continue to produce 4n individuals, if mates with only 2n

-won't work if self-fertilizes, mates with 4n sibling, or backcrosses to parent.

if backcross.... produces 3n which is sterile

table 5.2!!

-point mutations

-inversions

-duplications

-polyploidy

Summar Statistics:

1)halotype diversity (ie. haploid genotypes: mitochondria)

2)allelic diversity (expected heterozygosity)

-look at heterozygosity (h) to measure variation

-hexp= 1sumX^2 (x=frequency of each allele at one locus)

polymorphism (another word for variation): multiple alleles at a single locus

classical model-

-mutations are good or bad (selected for or against)

-low levels of polymorphism

-wrong

balance/selectionist model

-lots of polymorphism, stable in number of alleles

-natural selection.. frequency of alleles changes

-ie. host parasite co-evolution

neutral model

-alleles functionally and selectively equivalent

-drift

-selection does not dictate frequency of alleles

*vertebrate heterozyosity is around 0.08-0.1 on average, while inverts are much more distributed

N E.Seals hunted to near extinction

-South ones were not... harder to access

-there were about 8 north ones left (bottleneck)

-now over 125000 again

NORTH E.SEAL

-hunted until 1884

-in 1892 8-20 seals

-179bp mt control regions

-5 haplotypes pre-bottleneck (looked @5, found 5)

-2 post-bottleneck (huge pop size)

Nvs.S

-genetic drift led to a loss of variation in North

-population cannot evolve as well is respone to changes

-S has way more haplotypes

Phenotypic Variation

-What determines the phenotype?

1)genotype does

2)environment does (AA flower could be red here pink there)

3)maternal effects (red flowers if parent 2yrs, pink if mother is 4

4)genomic imprinting

Genetic Variation

Sources:

1)mutation (produce new alleles)

2)recombination (linked genes.. new combination of different phenotypes)

3)gene flow

4)hybridization (can result in endless amounts of variation

Human susceptibility to flatworm infection influenced by single gene (SM1)

-pedigree analysis

-2 codominant alleles S and R

SS = susceptible

RR = resistant

SR = intermediate

*more variation means better ability to adapt

*maintained by mutation, selection, ec

selection will select for non-synonymous mutations in smaller organisms due to shorter generation time and other factors

Early studies using protein electrophoresis.

Non-denatured proteins migrate at different rates due toL

1)changes in a.a.

2)changes in pH

3)size

4)shape

Adh (alcohol dehydrogenase)

-metabolizes alcohol... has 2 alleles

F (fast on gel)

S (slow on gel)

-each adapted to specific environment (Drosophila)

-stability of idfferent alleles at different temperature

Fundulus

-lactate dehydrogenase B

-job is to break down lactate into pyruvate

-there are 2 alleles

-frequency of alleles varies strongly with latitude (warm-cold)

-this is due to stability of proteins

DNA polymorphisms

-non-synonymous (dN)... changes a.a.

-synonymous (dS).. do not change

-dN/dS ratio tells us if evolution at a locus is due to:

1)drift... dN/dS=1

2)negative/purifying selection (<1)

3)positive/diversifying selection (>1)

-"important" loci evolve slowly (low dN/dS)

-neutral or unimportant loci evolve quickly via drift

-few loci, diversifying selection (host antibodies, antigen proteins in viruses)

-gene n human chromosome 3

-encodes cell surface protein on white blood cells

-binds to chemokins (released by other immune cells), WBC moves to infected area

HIV1 uses CCR5 as co-receptor

-certain CCR5 alleles (delta32) make individuals less susceptible to strains of HIV1

-when 32bp deletion causes CCR5 to become non-functional... HIV1 canot bind to the WBC, no infection

delta32/delta32 = resistant to most strains

delta32/+ = susceptible, but slow progression to AIDS

+/+ = susceptible

-test individuals using PCR to see if susceptible

Can we use phenotype to determine genotype?

-only when single gene

-DNA is more powerful

CF (cystic fibrosis)

-CFTR gene: cell surface protein expressed in lung membranes

-one function is to ingest or destroy Pseudomonas

-individuals with mutation in CFTR have CF

-out of 15000 patients, 500 different mutations

-all same phenotype

-all have CF

population: group of potentially interbreeding individuals and their offspring

evolution: change in allele frequencies over time (across generatiions)

population genetics: combines natural selection with mendelian genetics

Allele frequencies in a population will only stay the same (HW equilibrium) if several assumptions hold true:

1)no net mutations

2)no migration (no gene flow b/w populations)

3)random mating (allele frequencies do not change, genotypes may change)

4)population is very large (no genetic drift)

5)no selection (all survive and have equal fitness)

Under HW, allele frequencies do not change, and evolution does not occur.

EQUATION:

p^2 + 2pq + q^2 = 1

p^2 = probability of AA

q^2 = probability of aa

-to get probability, multiply frequencies of alleles)

Use Chi-squared test to determine if observed frequencies are significantly different from expected frequencies

Chi squared = sum (O-E)^2/E

***If chi stat is greater than Pcrit (critical value), then observed is significantly different from expected.

*****Whether an allele is common or rare is independent of dominant and recessive

******violations of HW equilibrium are agents of evolutionary change

1)mutations

2)gene flow

3)non-random mating

4)genetic drift (founder effects, bottlenecks)

5)selection

-variation present

-individual variation causes differential fitness

-variation inherited

Individuals with certain phenotypes have higher survival OR increased fitness (phenotype must be heritable)

Results in some individuals having more offspring than others

Problems:

-environmental influences

-multigenes

-continuous traits (vs discrete)

(cont. would be weight in humans, disc would be red or white flowers)

INDUSTRIAL MELANISM

-camo of moths during industrial period

-moths land on limbs

-in polluted woodland, more white are eaten, in nonpulluted woodland, more melanic are eaten

*If starting frequencies are the same, and there is equal selection, frequencies will not change, and there will be no evolution*

*when there is equal selection on homozygotes, and same number of each to start, genotype frequencies are affected but not allele frequencies.

* selection on only heterozygotes will also not change allele frequencies

For each genotype:

-average absolute fitness W

-relative fitness w

-by definition, best genotype has w=1

-all others w=W/Wmax

w=1 = zero selection

w = 0.75 = 25% selection

s=1-w

-the rate of genetic change under selection depends on relative, not absolute fitness

-relative fitness defines the fitness of genotypes relative to the best genotype and it defines the selection coefficient "s"

-recessive rare: evolution by selection is slow

-dominant rare: evolution by selection is fast!

Drosophila

-2 experimental populations with ethanol food

-2 exp pops with normal food

-randomly selected breeders for each generation (create new population)

-each generation determined genotype and allele frequencies (AdhF and AdhS alleles)

-all started with 35% AdhF

-control had no change in frequencies

-expt had rapid increase in frequency of AdhF

PATTERN OF SELECTION (next exp)

-recessive vs dominant allele

-two alleles: +wild type and l(lethal)

+/+ and +/l is normal

l/l is lethal

-two populations of heterozygotes, measure change in allele frequencies over time

-started with 100% heterozygotes

-gets smaller and smaller % with lethal allele

WILL NEVER GO EXTINCT!! (always will be hetero)

*if ther is selection for a rare allele, it will slowly increase in frequency and then suddenly over take the other allele, going to nearly 100%, but will never get fixation

*only selection for a recessive allele can cause fixation (or a bottleneck)

Compound chromosomes (Drosophila) have problems with segregation during meiosis

-sperm and eggs are either full, empty of all of one chromosome

-crossing to inferiors together yields 1/4 viable offspring

-crossing with a normal yields no viable offspring (cannot match)

Genotype's succes depends on its frequency

-positive frequency dependence favours common form

---aposematic/warning colouration (monarchs)

-negative frequency dependence favours rare form

---host-pathogen evolution

---self incompatibiliy alleles in plants

ELDERFLOWER ORCHID

-yellow or purple flower

-pollinated by bumblebees

-no reward for bee

-bees visit equal numbers of yellow and purple flowers

-less frequent flowers have higher reproductive success

SNAILS AND TREMATODES

-sympatric parasites (same pond) and allopatric parasites (different ponds)

-way higher infection in sympatric parasites

*selection will afect the rate of mutation depending on whether it is advantageous or deleterious

EXP>.

Greq E.coli on minimal media

-repeated transfer 10000 generations (4+years)

-periodically froze samples (to compare relative fitness later)

-combined frozen samples with descendents to measure fitness

-over the course of 1000s of generations, every once in awhile there would be a sudden increase in cell size (advantageous mutation, which becomes fixed to high frequency)

THEORY- Mutation-Selection Balance

-loss of deleterious alleles by selection equals production of deleterious alleles through mutation

at equilibrium: q=SQRT(u/s)

q=equilibrium frequency

u=mutation rate

s=selection coefficient (0=no selection, 1=all die)

-if s is small, u is high... q is higher (producing at higher rate than removing)

-if s is large, and u is low, q is lower

definition????

Many genes encode leucine.. through synonymous mutation

-highly expressed genes can produce more protein... where one of the leucine producing genes is very prevalent compared to the others.

-lowly expressed genes occur when function of protein is not as critical. Can't produce as much... many different genes can produce leucine.

-tRNAs that add to create leucine are different in frequency

Why is codon bias related to gene expression?

Neurodegenerative disease (muscle stop working)

-most common recessive autosomal fatal disease

-telSMN mutation(s) on chromosome 5

-mutatn alleles 1/100 in caucasians

s=0.9

0.01=SQRT(u/0.9)

u=0.0004 (high)

Why are disease causing alleles so frequent?

-very strong selection against

-but very high mutation rate

-found that 7/340 had mutation (0.0011)

-this is actual, 0.0004 is theoretical

CFTR cell surface protein

-ingest and destroy Pseudomonas

CF alleles 0.02 Europeans (2%.. very high)

-infertile... alleles cannot be passed on (s=1)

-predicted mutation rate is 0.004), actual is 25 fold lower

-so what is keeping frequency of disease causing alleles so high?????

*confers resistance to somthing else!!

Typhoid fever! (doesn't infect cell lining, but intestinal lining)

-are CF heterozygotes resistant?

-bacteria infect cell via gut lining

 -perhaps using CFTR protein?

-copy number

Looked at deltaF508 (1bp deletion)

-maybe CFTR gene allows port of entry?

-most common within CFTR gene

-many different mutations cause CF

-found heterozygote advantage!! (in mice)

-86% decrease in infection from wildtype to heterozygote (+/deltaF508)

-wildtype has extremely high rate of infection

-found very strong correlation in humans between number of typhoid cases and %mutant alleles that are deltaF508

dN/dS increases in mammal phylogenetic tree until it peaks at humans and chimps for this gene

BRCA1 is a tumor suppressor gene

Exon 11 is one part of the gene

-more non-synonymous mutations occurring in humans and chimps... new thing can maybe select against tumors

def: movment of alleles between populations (gene flow)

technical def: seasonal movement between two home-ranges of an organism

Migration includes dispersal of individuals or gametes

-internal vs external fertilization (dif potentials of dispersal)

-dispersal agents (plants have higher potential)

-barriers (what will prevent it?)

*models assume all populations have same #individuals (N) and equal migration rates (m)

Stepping stone model (movement between populations next in line (1-3 is indirect)

Island model

One island model (asymmetrical migration

Depends on:

-population size

-number of migrants

Rate of Change proportional to:

-migration rate

-direction of gene flow

-population differences in allele frequencies

*gene flow prevents differentiation/divergence b/w populations

**starting allele frequencies make a big difference. If two populations are homozygous for difference alleles, then rate of change will be very large compared to if the populations are similar in allele frequencies**

-single locus... A_ banded and aa unbanded

-found ore unbandedness on island populations

-baksing behaviour on islands... predators and unbanded are more cryptic

-suggests that selection favors unbanded snakes on islands

-Why is banded allele not lost from island populations? (unbanded is recessive)

-migration from mainland!

-a statistic used to measure population differentiation

-0 means no structure and high gene flow

-1 means fixed differences and no gene flow

-loots at allele frequencies and says if they're different

CAMPION (red bladder)

-series of different aged islands (isostatic rebound)

-plant dispersed via wind and water

-is an early colonist

prediction:

-Young populations have lots of variation in allele frequencies due to chance

-Intermediate populations homogeneous due to migration

-Old populations structured, random survival

-looked at 52 islands and 6 loci

-found that yong populations had greatest variation

-intermediate populations were lower than average and had less variance

-old populations also had low variance

Mark recapture

-time consuming

-limited returns

Satellite tags

-small N

-limited time

-can't measure gene flow

-expensive

-battery life

-only looks at movement, not gene flow

-don't know what they are doing

Genetic Markers

-long period of time... 10s of thousands of years

-gene flow in both directions is not equal

-non-linear relationship b/w Fst and Nm (assumes gene flow occurs bidirectionally and equally)

Nm is the net # migrants

=

migration rate*population size

Genetic Drift is a "random" element in evolution

-it is making a population smaller due to random change

-allele frequencies in population change from generation to generation due to chance

*Drift can act on gametes or individuals

-cannot produce adaptation (selection does this)

-can lead to fixation of alleles

-drift may cause selection to occurr

*small population = big fluctuations!

CAUSES
population bottlenecks: events that RANDOMLY remove most members of the population (ie. a flood)

founder effects: processes that RANDOMLY disperse a small number of individuals to a new location. These individuals form the new population (blown to island)

*effects are stronger and occur faster in small population

*over time there is a large change in allele frequencies

*Because fluctuations are random,

---each population has unique trajectory,

---fixation/loss of some alleles occurs,

---frequency of heterozygotes decreases

***fixation/extinction of allele occurs much sooner in small population that in large population

migration:

-inreases population variation

-decreases differences among population

drift:

-decreases population variation

-increases differences among population

SILVER EYES
-wing length is different in different populations

-**allelelic diversity decreases  in colonized areas

-bottleneck occurs at each colonization

BOTTLENECK confounding factors:

-#colonizers

-sex ratio

-distance of island

-population size

What is the probability that a given allele will become fixed, related to allele frequency?

x/2N (x=# copies of specific allele)

***same as initial allele frequency

**heterozygosity decreases at a much greater rate in a small population size

Max heterozygosity occurs whenfrequency of both alleles is 50%

Drosophila

-107 populations... 8M and 8F in each pop (16N)

-All hetero for brown gene (bw75/bw)

-**3 phenotypes for this locus

-created multiple bottlenecks through subsampling (kept removing 8/8(16) from each consecutive population)

-by 19th generation, bw75 was fixed in 28 populations and lost in 30 populations

-heterozygosity decreased on average

-most populations lost genetic diversity

***heterozygosit decreased at a faster rate than expected!

-census population was 16 (not all individuals reproduced!)

-effective population was 9 (average)

Size of an ideal, randomly mating population that would lose genetic variation via drift at the same rate as it is observed in the population (no sampling errors)

Ne= (4NmNf)/(Nm+Nf)

MALE PRAIRIE CHICKENS

-lek mating system

-population crash in 1994 (bottleneck)

*alleic diversity lost faster than heterozygosity

*rare alleles lost quickly (frequency of allele and population size directly affect probability of allelic retention)

On 6 loci, pre-bottleneck # of alleles was 5.12, while after it was 3.67

What caused hatchability to decrease?

-mutational meltdown (mutation, population size, and drift)

-migration decreased by habitat fragmentation

*****

Extinction Vortex: bottleneck caused decreased population size, which in turn caused decreased fitness and increased rate of drift, which in turn caused increased rate of fixation of deleterious alleles

Assortative mating

-not random phenotypic

-look for characteristics

(snow geese color morphs)

inbreeding

-selfing in plants

-mating with relatives (consanguineous)

F

probability that two alleles are identical by descent

F=0=no inbreeding

F=0.5=complete...selfing (can only share up to 50% with self)

homozygote: A_iA_i=P_i²(1-F)+p_iF

heterozygote: A_iA_j=2p_ip_j(1-F)

p_i and p_j are frequencies of i and j allele

**look at trees Jan29 lecture and understand math!!

inbreeding depression = 1-(ws/wo)

ws=fitness of selfed individuals

wo-fitness of outcrossed

-easiest to measure when individual is stressed

-appear later in life (maternal effect?)

-varies among lineages (allele dependent)

0=no inbreeding dependency

1=max

Why is inbreeding bad?

What causes it?

How can you reduce it?

Why is inbreeding bad?

-loss of diversity

-accumulation of deleterious alleles

What causes it?

-isolation

-small density

-decrease in population size

How can you reduce it?

-migration

-self incompatibility

-captive breeding

Genotype: yes

Allele: no

**no evolution for inbreeding on its own**

If all individuals reproduce by selfing, number of heterozygotes wil half each time

-hunted to near extinction

-did decrease population size and density also lead to inbreeding?

-screned 31 loci including PAP

-PAP has 2 alleles

-SS=16, SF=7, FF=10 (allozymes... fast and slow)

*look at observed frequencies, and expected under HWE

Not in HWE.. .other explanations?

-Wahlund effect

-heterozygote disadvantage

-inbreeding

Mate choice

-MHC (major histocompatibility complex) ... scent relatedness (do they smell like you?)

Self imcompatability genes

-dispersal

-in small populations, avoidance is not possible

*Non-random mating can result in changes in allele frequencies, but not directly

nonrandome mating --> genotype frequencies -->phenotype frequencies --> selection

******nonrandom mating on its own does not result in evolution

Deleterious alleles appear and are removed

Neutral mutations fixed or lost via drift

Advantageous alleles appear and are fixed

WHY WORRY ABOUT DRIFT/MIGRATION/INBREEDING?

short term:

-increased homozygosity due to drift or inbreeding can expose deleterious recessive allels

Long term:

-alleles lost via drift reduces ability to adapt

Conservation!