Download Non-random Allelic Variation

Non-random Allelic Variation
AKA
Natural Selection
Adaptation
– a derived character that evolved in response to a specific
selective agent (although traits evolve from pre-existing ones
and selective agents change in time)
or
– a feature that is maintained because of natural selection for
its function
preadaptation – a trait that fortuitously serves a new function
adaptation is non-random or directional evolution
adaptation results from selection
selection can only act on existing variation
most adaptations are modifications of pre-existing ones
therefore, its results are most often ‘retro-fitted’ and some are suboptimally designed and can only be understood in the context of how
they came to be
adaptation results from selection
Selection defined
Wright: “any process in a population that alters gene frequency in a
directed fashion without a change in genetic material”
Futuyma: “any consistent difference in fitness (i.e., survival and
reproduction) among phenotypically different biological entities [be
they genes, species, or groups]”
“directed” and “consistent” distinguish selection from drift, from
randomness
Selection is mathematically related to fitness – a measure of
reproductive output with no other connotation
Most people equate evolution with adaptation
In fact, much of evolution is not adaptive
Non-adaptive traits include those due to
consequences of physics or chemistry, e.g., blood is red
drift
linkage or ‘genetic hitchhiking’
pleiotropy
phylogenetic history
Natural Selection  Evolution
evolution is a two step process
1) origin of genetic variation
2) change in the frequency of alleles and genotypes
evolution can occur in the absence of natural selection
natural selection can occur without evolution resulting
natural selection acts on phenotypes, but evolution describes a
change in genotype
thus, the degree to which selection results in evolution
depends on the heritability (i.e., % genetic variance) of a trait
Selection is mathematically related to fitness
Selection acts on the phenotype of individuals but, to the
extent that selection can be an evolutionary force changing
genotype frequency, it is the average reproductive success of
heritable phenotypes that counts
after all, there may be non-selective deaths of individuals
with genotypes of otherwise high average fitness
Reductionist view of selection
Richard Dawkins The Selfish Gene 1989
“a coach selects a team of oarsmen for a crew race by repeatedly
shifting oarsmen among several boats and racing them, after several
trials the winning boat will have all the same oarsmen. A crew
member finally chosen will have been grouped with both good and
inferior ones at different times, but on average his performance has
contributed more to the trials than one who was not chosen. Natural
selection within populations can be understood as competition
among alleles, the winner being the one that confers some
characteristic on an organism that provides the allele with the highest
rate of survival and reproduction, averaged over all gene
combinations in which the allele occurs”
Levels of selection
Genic selection
Individual selection
Kin selection
Group selection
Species selection
It is self-evident that selection acts at different levels
because these may be in mutual conflict
Genic selection – potentially detrimental to the individual
e.g., lethal recessive t-allele in mice,
frequency 40% in wild populations but
present in >90% of sperm due to
segregation distortion
e.g., medea allele in flour beetles,
lethal to heterozygous offspring of
mother that has it, therefore ensuring
father has it too
e.g., retrotransposons or “selfish
genes” such as Alu I that may cause
somatic cancers or disorders such as
neurofribromatosis type 1
In the case of genic selection, we certainly don’t imagine that the tallele or Alu 1 retrotransposon is making a conscious decision or
planning its own increase
it is simply that through some mechanism of mutation a variant
appeared at some time in the past that conferred an ability for the
gene to reproduce itself or to reproduce itself more rapidly, and so
it did
thus, what we describe as selection is simply the consequence of a
reproductive advantage
stated differently, selection has no forethought
if it had, then the t-allele or Alu 1 retrotransposon might realize
that by increasing its own reproductive success in the short term it
negatively impacts the organism it depends on to survive in the
long term
Individual selection – potentially detrimental to the species
e.g., “cheaters” or individuals who deceive others for personal gain
e.g., infanticide in lions, rats, various birds
Does a male lion that just claimed a pride decide to kill existing
cubs specifically because he consciously wants to optimize his
reproductive success relative to other genotypes?
probably not
Again, without forethought, “selection favors” a particular
phenotype (in this case a behavior) because it has the result of
improving the reproductive output of individuals that trait
relative to those that do not
Kin selection
i.e., assisting the reproductive success of relatives to improve one’s
own inclusive fitness (the notion that an individual’s fitness is
increased by the fitness of all who share his or her genes)
e.g., delayed dispersal of young and
cooperative breeding in a variety of
birds, such as Harris’ hawks, acorn
woodpeckers, scrub jays, ,
choughs, white-fronted bee-eaters
But appearances may be deceiving
Genotyping has revealed what goes on behind closed doors and
within nesting cavities
nest helpers are sometimes cuckolders
moreover, some offspring choose to become nest helpers only
after their own attempt at nesting was sabotaged
- by their own parents!
Altruism and Group Selection vs Kin Selection
Altruism – an act for the benefit of another with potential cost and no
expectation of personal reward (including inclusive fitness)
Altruism is unlikely to evolve due to natural selection because there is
no heritable fitness advantage to the provider; but it can result as a
‘unintended’ or ‘misdirected’ consequence of another selected trait
Altruism and Group Selection vs Kin Selection
Group selection – like altruism, group selection acts for the benefit of
a group of individuals that are not necessarily related
Group selection is unlikely to evolve due to natural selection or drift
because the effective population size of the group is larger than the
lineage of the selfish individual (“cheater”) who derives an
immediate fitness benefit and whose lineage can evolve more
rapidly to exploit altruistic behaviors of the group
Species selection
e.g., extinction of species with little genetic variation
e.g., evolution of sex ratios
and population densities
Selection is mathematically related to fitness
Fitness of a genotype – average of fitnesses of all individuals
of the genotype, or “the average per capita lifetime
contribution of individuals of that genotype to the population
after one or more generations”
i
i
𝑅 – absolute fitness of genotype i.e., per capita growth rate of
genotype
i
i
𝑅 = (fraction of offspring of genotypei surviving to reproduce) X (average fecundity)
(WARNING: there are alternative definitions of absolute fitness – avoid confusion, beware the internet)
𝑅 - average per capita growth rate of population (the equivalent of
the intrinsic growth rate “r” of a given genotype but for clonally
reproducing species with non-overlapping generations)
i
i
𝑊 – “relative fitness” i.e., value of 𝑅 relative to the absolute fitness
of the maximally fit genotype 𝑅MAX
i
𝑊
i
𝑅
=
< 1.0
𝑅MAX
𝑅MAX
𝑊MAX =
= 1.0
𝑅MAX
The rate of genetic change under selection depends on the
relative, not absolute, fitnesses of the genotypes
𝑅i
number of individuals 
𝑅MAX
t=1
t=2
generations 
Different relative fitnesses yield different relative growth rates
𝑤 - “average fitness” i.e., the average fitness of individuals in the
population relative to the maximally fit genotype
𝑤 = (𝑊 11)(frequency11) + (𝑊 12)(frequency12) + (𝑊 22)(frequency22)
example
Given:
Genotype frequencies
A1A1 = 20%
A1A2 = 30%
A2A2 = 50%
Absolute fitnesses
𝑅11 = 6
𝑅12 = 8
𝑅22 = 10
Relative fitnesses
6
𝑊 11 = 10
= 0.6
8
𝑊 12 = 10
= 0.8
𝑊 22 = 10
= 1.0 = 𝑊 MAX
10
Average fitness
𝑤 = (𝑊 11)(frequency11) + (𝑊 12)(frequency12) + (𝑊 22)(frequency22)
𝑤 = (0.6)(0.2)+(0.8)(0.3)+(1)(0.5) = (0.12)+(0.24)+(0.5) = 0.86
example
Given:
Genotype frequencies
A1A1 = 20%
A1A2 = 30%
A2A2 = 50%
Absolute fitnesses
𝑅11 = 6
𝑅12 = 8
𝑅22 = 10
Relative fitnesses
6
𝑊 11 = 10
= 0.6
8
𝑊 12 = 10
= 0.8
𝑊 22 = 10
= 1.0 = 𝑊 MAX
10
Average fitness
𝑤 = (𝑊 11)(frequency11) + (𝑊 12)(frequency12) + (𝑊 22)(frequency22)
𝑤 = (0.6)(0.2)+(0.8)(0.3)+(1)(0.5) = (0.12)+(0.24)+(0.5) = 0.86
example
Given:
Genotype frequencies
A1A1 = 20%
A1A2 = 30%
A2A2 = 50%
Absolute fitnesses
𝑅11 = 6
𝑅12 = 8
𝑅22 = 10
Relative fitnesses
6
𝑊 11 = 10
= 0.6
8
𝑊 12 = 10
= 0.8
𝑊 22 = 10
= 1.0 = 𝑊 MAX
10
Average fitness
𝑤 = (𝑊 11)(frequency11) + (𝑊 12)(frequency12) + (𝑊 22)(frequency22)
𝑤 = (0.6)(0.2)+(0.8)(0.3)+(1)(0.5) = (0.12)+(0.24)+(0.5) = 0.86
example
Given:
Genotype frequencies
A1A1 = 20%
A1A2 = 30%
A2A2 = 50%
Absolute fitnesses
𝑅11 = 6
𝑅12 = 8
𝑅22 = 10
Relative fitnesses
6
𝑊 11 = 10
= 0.6
8
𝑊 12 = 10
= 0.8
𝑊 22 = 10
= 1.0 = 𝑊 MAX
10
Average fitness
𝑤 = (𝑊 11)(frequency11) + (𝑊 12)(frequency12) + (𝑊 22)(frequency22)
𝑤 = (0.6)(0.2)+(0.8)(0.3)+(1)(0.5) = (0.12)+(0.24)+(0.5) = 0.86
example
Given:
Genotype frequencies
A1A1 = 20%
A1A2 = 30%
A2A2 = 50%
Absolute fitnesses
𝑅11 = 6
𝑅12 = 8
𝑅22 = 10
Relative fitnesses
6
𝑊 11 = 10
= 0.6
8
𝑊 12 = 10
= 0.8
𝑊 22 = 10
= 1.0 = 𝑊 MAX
10
Average fitness
𝑤 = (𝑊 11)(frequency11) + (𝑊 12)(frequency12) + (𝑊 22)(frequency22)
𝑤 = (0.6)(0.2)+(0.8)(0.3)+(1)(0.5) = (0.12)+(0.24)+(0.5) = 0.86
example
Given:
Genotype frequencies
A1A1 = 20%
A1A2 = 30%
A2A2 = 50%
Absolute fitnesses
𝑅11 = 6
𝑅12 = 8
𝑅22 = 10
Relative fitnesses
6
𝑊 11 = 10
= 0.6
8
𝑊 12 = 10
= 0.8
𝑊 22 = 10
= 1.0 = 𝑊 MAX
10
Average fitness
𝑤 = (𝑊 11)(frequency11) + (𝑊 12)(frequency12) + (𝑊 22)(frequency22)
𝑤 = (0.6)(0.2)+(0.8)(0.3)+(1)(0.5) = (0.12)+(0.24)+(0.5) = 0.86
example
Given:
Genotype frequencies
A1A1 = 20%
A1A2 = 30%
A2A2 = 50%
Absolute fitnesses
𝑅11 = 6
𝑅12 = 8
𝑅22 = 10
Relative fitnesses
6
𝑊 11 = 10
= 0.6
8
𝑊 12 = 10
= 0.8
𝑊 22 = 10
= 1.0 = 𝑊 MAX
10
Average fitness
𝑤 = (𝑊 11)(frequency11) + (𝑊 12)(frequency12) + (𝑊 22)(frequency22)
𝑤 = (0.6)(0.2)+(0.8)(0.3)+(1)(0.5) = (0.12)+(0.24)+(0.5) = 0.86
example
Given:
Genotype frequencies
A1A1 = 20%
A1A2 = 30%
A2A2 = 50%
Absolute fitnesses
𝑅11 = 6
𝑅12 = 8
𝑅22 = 10
Relative fitnesses
6
𝑊 11 = 10
= 0.6
8
𝑊 12 = 10
= 0.8
𝑊 22 = 10
= 1.0 = 𝑊 MAX
10
Average fitness
𝑤 = (𝑊 11)(frequency11) + (𝑊 12)(frequency12) + (𝑊 22)(frequency22)
𝑤 = (0.6)(0.2)+(0.8)(0.3)+(1)(0.5) = (0.12)+(0.24)+(0.5) = 0.86
Coefficient of Selection (𝑠i)
The intensity of selection against a less fit genotype, or
the selective advantage of a more fit genotype
i
i
𝑠 = 𝑊MAX − 𝑊
previous example, selection against A1A2 (or for A2A2 relative to A1A2)
𝑠22 = 1.0 − 0.8 = 0.2
With selection, allele frequency will change
Example using haploid with alleles A and B, with selection against A
′
𝑝 =
𝑞𝑅𝐴
𝑤
=
𝑞𝑅𝐴
𝑞𝑅𝐴 +𝑞𝑅𝐵
∆𝑝 = 𝑝′ − 𝑝
−𝑠𝑝𝑞
∆𝑝 =
1 − 𝑠𝑝
(note this equation applies only to this case)
p is negative if s, p, and q are positive
The absolute value of p is greatest when s is large and p = q
p slows as p  0
For diploids with alleles A1 and A2
𝑝′ =
=
1
2
freq𝐴1 𝐴1 𝑤11 + freq𝐴1 𝐴2 𝑤12
𝑤
𝑝2 𝑤11 + 1𝑝𝑞 𝑤12
𝑝2 𝑤11 + 2𝑝𝑞 𝑤12 + 𝑞 2 𝑤22
this equation will always apply to a di-allelic locus in diploids
(memorize it)
Modes of Selection
directional or purifying
𝒔
𝑝
stabilizing or normalizing
𝒕
𝒔
diversifying or disruptive
𝒔
Directional Selection with intermediate heterozygote fitness
directional
𝒔
𝑝
genotype
genotype frequency
relative fitness
∆𝑝 =
1
𝑠𝑝𝑞
2
1−𝑠𝑞
A1A1
p2
1
A1A2
2pq
𝑠
1-( )
2
A2A2
q2
1-𝑠
(where 1 − 𝑠𝑞 = 𝑤 ; note this equation applies only to this case)
Rate of change (∆) is maximal when 𝑝 = q = 0.5 (at any given s)
Rate of change (∆) is minimal as q  0
Directional Selection with dominance
directional
𝒔
𝑝
genotype
relative fitness
∆𝑝 =
𝑠𝑝𝑞 2
1−𝑠𝑞 2
A1A1
1
A1A2
1
A2A2
1-𝑠
(where 1 − 𝑠𝑞 2 = 𝑤 ; note this equation applies only to this case)
Even the slightest positive 𝑠 will result in fixation of the A1 allele
Rate of change (∆) is maximal when 𝑝 = ⅓ and q = ⅔
∆ decreases as q  0 because the denominator (𝑤 or average fitness)
increases
Directional Selection with dominance
directional
𝒔
𝑝
Recessive alleles are shielded from selection as q  0 because rare
alleles exist almost exclusively in the heterozygous state
Rare deleterious recessive alleles exist at low frequencies at many loci
Rare advantageous recessive alleles are also shielded from positive
selection, therefore initial increase in their frequency is expected to be
slow and may be dependent on drift
∆𝑝 equations using 𝑠 differ with every mode of selection
(so don’t memorize one and expect it to work for all problems)
stabilizing or normalizing
𝒔
𝒕
genotype
fitness
A1A1
1-𝑠
A1A2
1
A2A2
1-𝑡
diversifying or disruptive
𝒔
genotype
fitness
A1A1
1
A1A2
1-𝑠
A2A2
1
MRSA - Methicillin-resistant Staphylococcus aureus
VRE - Vancomycin-resistant Enterococci
FQRP - Fluoroquinolone-Resistant Pseudomonas aeruginosa
Nature 497, 24–26 (02 May 2013) doi:10.1038/497024a
Persistence of Polymorphism
If selection fixes alleles then why is there polymorphism?
1) Recurrent mutation
2) Gene flow
3) Genetic drift
4) Balancing selection
Persistence of polymorphism by recurrent mutation
mutation A1  A2
𝑞=
𝝁
𝒔
Where
𝑞 = equilibrium frequency of A2 (the mutant allele)
𝝁 = mutation rate
𝒔 = selection coefficient
Don’t memorize the equation
Remember that the ratio of the numerator to the denominator is what
determines the equilibrium frequency of the mutant
>1,800 distinct mutations in CFTR gene cause cystic fibrosis
Persistence of polymorphism by gene flow
A2 is advantageous elsewhere
𝑞∝
𝑚 𝑞𝑚
𝑠
Where
𝑞 = equilibrium frequency of A2
𝑚 = rate of gene flow
𝑞𝑚 = frequency of allele among immigrants
If rate of gene flow 𝑚 >> 𝑠, then populations won’t differentiate
Don’t memorize the equation
Remember that the ratio of the numerator to the denominator is what
determines the equilibrium frequency of the mutant
Persistence of polymorphism by gene flow
Cline – continuous or monotonic change in allele frequency along a
geographic transect; the hallmark of gene flow
Clinal variation in aminopeptidase
gene in mussels (Mytilus edulis) in
Long Island Sound
seawater
Long Island Sound
Hudson River
brackish water
Long Island
Atlantic Ocean
Clinal variation in SNP in human HERC2 intron for blue-brown eye color
Balancing Selection
(not mutually exclusive of normalizing and disruptive selection)
Types
1) Heterozygote advantage
2) Antagonistic selection
3) Varying selection
3a) Temporal
3b) Spatial
4) Inverse Frequency dependent selection
Heterozygote Advantage (hybrid vigor, heterosis)
Selection “for” the heterozygote
genotype
fitness
A1A1
1-𝑠
A1A2
1
A2A2
1-𝑡
Equilibrium frequency of allele = selection against the other allele
divided by the sum of selection against both alleles
Equilibrium frequency of A1 = 𝑝
Equilibrium frequency of A2 = 𝑞
𝑝=
𝑡
𝑠+𝑡
𝑞=
𝑠
𝑠+𝑡
Equilibrium frequencies depend on a balance of fitnesses of A1A1
and A2A2
Hybrid vigor
most cases of heterozygote advantage are equivocal, and may simply
represent inbreeding depression
hybrid
inbred
inbred
Antagonistic Selection
selection “against” the homozygotes
truly no different than heterozygote advantage because selection
for one genotype is selection against another
genotype
fitness
A1A1
1-𝑠
A1A2
1
A2A2
1-𝑡
Antagonistic Selection – Sickle Cell hemoglobin allele
“Sickle cell disease is the most common inherited blood disorder in the United States, affecting
70,000 to 80,000 Americans. The disease is estimated to occur in 1 in 500 African Americans
and 1 in 1,000 to 1,400 Hispanic Americans” (US Natl Lib Med)
Selection against homozygous wild type hemoglobin genotype –
no malaria resistance
Selection against homozygous sickle cell hemoglobin genotype –
vaso-occlusive crisis, hemolysis, anemia, and complications
Selection for heterozygote in geographic areas of malaria endemism –
malaria resistance
Anopheles mosquito vector
current distribution of malaria
Selective agent – Plasmodium falciparum protozoan
Selection against wild type hemoglobin homozygote
Selection for sickle cell hemoglobin heterozygote in areas of malaria
endemism
Plasmodium falciparum gametocytes
Selection against sickle cell homozygote everywhere
Normal RBC
Sickled RBC
Varying Selection
typically, individuals do not experience multiple environments
Temporally varying environmental conditions
different phenotypes are selected for or against at different
times
requires heterozygote disadvantage
Spatially varying selection
“multiple niche polymorphism” or “habitat selection”
different phenotypes are selected for or against in
geographically different environments
model generally assumes limited gene flow between demes
Varying Selection
Apple Maggot Fly Rhagoletes pomonella
Spatially segregated on hawthorn and apple fruits
Temporally segregated by phenology of hawthorn and apple
fruiting
Inverse Frequency Dependent Selection
the rarer allele has a selective advantage, simply for being rarer
e.g., behavioral preference for non-self Major Histocompatibility
(MHC) alleles in mice
e.g., self-incompatibility S-alleles in flowering plants
Alternative Equilibria (not balancing)
Types
Positive Frequency Dependent Selection
Heterozygote Disadvantage (underdominance)
Adaptive (fitness) landscapes
Two types of frequency dependent selection
Fitness of genotype depends on genotype frequencies in the population
Inverse Frequency Dependent Selection – balancing, maintains polymorphism
Positive Frequency Dependent Selection – not balancing, alternative equilibria
Positive
Inverse
𝑤22
𝑤𝑖
𝑤11
𝑤12
𝑤12
𝑤22
0
p
1.0
0
𝑤11
p
1.0
Positive Frequency Dependent Selection in Heliconius butterflies
a “supergene” region for mimetic color pattern polymorphism without intermediates
(Joron et al 2006 PLoS Biol 4: e303)
Heterozygote Disadvantage or underdominance
initially more frequent allele will become fixed
𝑝 = 𝑞 is unstable
this differs from varying (and
Disruptive) selection because
there is gene flow
𝑤
unstable 𝑝
0
p
1.0
Heterozygote Disadvantage or underdominance
initially more frequent allele will become fixed
𝑝 = 𝑞 is unstable
this differs from varying (and
Disruptive) selection because
there is gene flow
𝑤
unstable 𝑝
0
p
1.0
Adaptive Fitness Landscapes
until now, we have considered only two-dimensional graphs of single
locus diallelic traits
Fitness landscape - a multi-dimensional representation of the average
fitness of populations with respect to polygenic traits (i.e., genotypes
controlled by two or more loci)
Graphing fitness of polygenic traits
genotype
relative fitness
A1A1
1
genotype
relative fitness
B1B1
1-𝑡
A1A2
𝑠
1-( )
2
B1B2
1
A2A2
1-𝑠
𝑤
𝑝
B2B2
1-𝑡
𝑤
𝑝
𝑤
𝑝A
𝑝B
𝑤 is weighted by the
frequency of each
genotype
in this example, there is only one maximally fit genotype, marked
𝑤
𝑝A
𝑝B
𝑤
𝑝A
𝑝B
but there can be multiple equally fit genotypes in a fitness landscape
especially if fitness of a phenotype is influenced by many loci or if
environmental conditions are varied
Since selection is measured as relative fitness, by definition selection
can only make populations “climb up” fitness landscapes
selection has no forethought; it cannot drive a population down a
fitness landscape to cross a “fitness valley” (of lesser average fitness)
even if it is to reach a peak of higher fitness
populations may be “stuck” in local optima even if they could
hypothetically optimize genotypes for even better average fitness
however, drift can alter allele frequencies in small populations
independently of selection, either up or down fitness gradients
because it is random
Transilience
the interaction of selection and drift that can drive a population
down a fitness gradient into and through an adaptive or fitness
“valley” across to a new fitness optimum
transilience is thought to be particularly important in the evolution
of founding populations, because
drift has a large effect in small populations sizes, and
founding populations may find themselves in novel
environments for which their existing genotype frequencies
are less than optimal
If traits can be non-adaptive, then how are
adaptations recognized?
Complexity
Suitability for function
Selection experiments
Comparative method
Methods of studying selection
1) Correlations among populations
H0 – variation is random
HA – variation is not random
e.g., latitudinal clinal variation in
ADH locus in Drosophila on both
sides of the equator
Methods of studying selection
2) Deviations from expected genotype frequencies
2a) H0 – Hardy-Weinberg Equilibrium
Caveat: there are other factors that can cause populations to not
be in H-W equilibrium
2b) linkage disequilibrium between traits that produce a suite of
functionally related characters despite their ability to be in linkage
equilibrium
Methods of studying selection
3) temporal patterns of stability or instability of polymorphisms
e.g. H0 – drift will cause fixation and monomorphy of alleles but
polymorphism is observed
e.g., HA – ∆𝑝 too fast to be accounted for by drift or neutrality
e.g., industrial melanism in peppered moth (Biston betularia)
Methods of studying selection
4) Response to environmental perturbations
e.g., change in bill dimensions of Medium ground (Geospiza fortis)
finch on Daphne Island, Galapagos after 1982 El Niño
Methods of studying selection
5) Genetic demography - relationship
of fitness or survival to phenotypic
variability
e.g., experimental manipulation
of tail length (attractive to
females) in Long-tailed
Widowbird (Euplectes progne)
video
Methods of studying selection
6) Functional studies
e.g., temperature affect on rate of enzyme activity, such as Taq DNA
polymerase in thermophilic bacteria (e.g., Thermophilus aquaticus)
Methods of studying selection
6) Functional studies
e.g., temperature dependence of enzymatic rate activity in Antarctic
Icefishes (Notothenioidei)
Methods of studying selection
6) Quantitative Trait Locus (QTL) Analysis
Polygenic traits with continuous phenotypic variability (vs discrete
phenotypes) and non-Mendelian patterns of inheritance
Mass selection on large populations can produce rapid phenotypic
effects outside the range of previously observed variation by bringing
together existing genetic variation and multiple alleles into novel
genetic combinations
QTL studies
e.g., William Castle’s experiments on pelage color in hooded rats
20 generations
QTL studies
aggressive vs domestic behavior in red fox (silver race)
40 generations
Methods of studying selection
6a) QTL mapping
linkage of trait in crossing experiments
best studied in plants and animals that can be rapidly and selectively
bred
6b) Genome Wide Association Studies (GWAS)
statistical correlation of SNPS and structural variants to one another
and to phenotype
best studied in relation to disease in humans due to availability of
many completely sequenced genomes, medical records, and interest
Methods of studying selection
7) Molecular studies
e.g., dN/dS ratio (nonsynonymous : synonymous substitutions)
e.g., substitution rates per codon position
e.g., codon bias