Evolution_9

changes at other loci that do not reduce the degree of resistance, but do reduce or eliminate the fitness costs associated with the resistant phenotype

one gene copy at each loci

• a. Darwin: natural Selection
• b. Mendel: genetic transmission

• Continuous: finely graded continuous characters essential for Darwin's theory of evolution
• Discontinuous: substantive discrete variations as studied by Mendel

traits affected by many genes simultaneously--first step in reconciling Darwinian natural selection with Mendel's inheritance b/c they can exhibit nearly continuous variation

inheritance of a polygenic trait (more complicated than simple Mendelian inheritance, but still predictable in a Mendelian framework)

• the phenotype can be calculated by summing the effects of each allele
• Example: more alleles for a darker color will give a darker phenotype

genetic reassortment draws out new phenotypes from preexisting variation (even in the absence of mutation)

alleles at two or more loci interact in a non-additive way to form a phenotype (the effect of one allele depends on which allele(s) are present at other loci)

the phenotypic effects of alleles at one locus depend on the context set by alleles at another locus

a defined set of alleles, one at each locus under consideration--set of gene copies along one particular chromosome (i.e. ABc or aBC, not AaBBCc)

alleles on the same chromosome--separate together unless recombination occurs (if they are closer together recombination is less likely to affect them)

choose mates that are similar

statistical linkage between alleles at two different loci (i.e. alleles at locus A and locus B)

difference between the actual frequency of the AB haplotype (hAB) and the expected frequency ( fA fB) of the same haplotype if the loci are independent—that is, if there is no association between the allele at one locus and the allele at the other (D=hAB - fA fB should be zero if independent)

when "like" alleles tend to couple in haplotypes (i.e. A with B and a with b)

when "opposite" alleles tend to occur together (i.e. A with b and a with B)--doesn't tend to happen

• Positive: excess coupling haplotypes
• Negative: excess repulsion haplotypes

• mutation (simplest source)
• selection (only for epistatic interactions)
• genetic drift (fluctuation and/or loss of haplotype)
• migration (intro of haplotypes--coupling, +D)

In the absence of evolutionary processes recombination will dissipate linkage disequilibrium (recombination usually occurs between haplotype pairs) -- deltaD= -rD

D= hAB hab - haB hAb (one half of frequency of coupling dbl heterozygotes - one half of frequency of repulsion dbl heterozygotes)

technique by which loci responsible for disease/other traits are located--rate at which disequilibrium breaks down between two loci is proportional to the distance between them along the chromosome (fundamental principle underlying association mapping)

allele frequencies at loci that are physically linked to the locus under selection may also change--an unselected or disadvantageous allele is able to "ride" along with a nearby favorable allele and increase in frequency (recombination will eventually decrease association between these alleles)

selection tends to eliminate genetic background on which deleterious alleles arise

• Alleles can increase in frequency due to selection either because they directly code for beneficial traits on their bearers, or because they are physically linked to other beneficial alleles at other loci
• Natural selection, be it positive or negative, tends to cause a decrease in genetic variation at loci near the selected allele

Result of tight linkage across entire bacterial genome: 1. New beneficial allele arises 2. fixation and selective sweep 3. new beneficial mutation arises and process repeats

when a beneficial mutation in bacteria is fixed, alleles at most other loci are also fixed because loci on bacterial chromosome are tightly linked

Periodic selection greatly reduces genetic diversity (before heterogeneity can build up by mutation, selective sweep eliminates it, occurs over and over, especially with bottlenecks)

slowing down of selection (beneficial mutations compete with each other for fixation)

Interactions among genes are important, generating a genotype to phenotype map--think about diff phenotypic or genotypic combinations as points on a map (consider fitness points as well)

a single gene affects multiple phenotypes

genes and environment interact in complex ways to determine phenotype

• 1. Pleiotropy
• 2. Epistasis
• 3. Norms of Reaction
• 4. Dominance
• 5. Multiple Pathways

one allele may cover up another allele at the same locus

A common phenotype may have a different genetic basis in different individuals

x- and y- axes represent the values of phenotypic traits (i.e. the size of a tree's leaves and the size of its flowers)--aspects of phenotype under consideration

combination of traits associated with the greatest fitness values

regions of lower fitness on fitness/adaptive landscape

genotypes that are mutational neighbors—namely, those separated by a single mutation—appear close together in the genotype space, whereas those that are separated by many mutations appear far apart (regardless of phenotypic differences)--not continuous because mutations are discrete

study of continuously varying traits--enables us to track not only the phenotypes of the individuals in the population, but also the variation that is present in the population, and whether or not this variation is heritable

Random chance events during development that give rise to considerable phenotypic differences (with the same genotypes)

• P is defined as the phenotypic value of the continuous trait being studied
• P= G + E (where G is due to genotype and E is due to environmental influence)

expected phenotypic value of the individuals with that genotype

deviation from P and G is attributed to environmental effects--expected E is zero because it is equally likely to be positive or negative

statistical measure of variation in a sample (larger variance means individuals differ more from each other and from the mean)

V_p = V_G + V_E

fraction of variance that is potentially heritable: H²=V_G / (V_G + V_E)

interactions between two alleles at the same locus

• A: additive component (sum of expected individual effects on each allele--independent of genetic background
• D: dominance component (sum of effects of dominance interactions between allele pairs at each locus)--depend on genetic background
• I: interaction/epistatic component: effects of epistatic interactions across loci--dependent on genetic background
• E: environment

fraction of total variation that is due to additive genetic variation (accessible to natural selection) : h²= V_A / (V_A+V_D+V_I+V_E)

relates the narrow-sense heritability, the strength of selection measured as S, and the consequences of selection measured as R: R=h²S (predicts evolutionary change for quantitative traits)

Heritabilities estimated from the selection differential and the selective response