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Chapter 6

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Department
Biology
Course
BIOL 359
Professor
Jonathan Witt
Semester
Winter

Description
BIOL359 - Evolution Winter 2013 Chapter 6: Mendelian Genetics in Populations I: Selection and Mutation as Mechanisms of Evolution - Population Genetics: Integrates Darwin’s Theory of Evolution by Natural Selection with Mendelian genetics o Changes in the relative abundance of traits in a population is tied to changes in the relative abundance of the alleles that influences them  Change across generations in the frequencies of alleles 6.1. Mendelian Genetics in Populations: The Hardy-Weinberg Equilibrium Principle - Population: Group of interbreeding individuals and their offspring - Adults  Gametes  Zygotes  Juveniles  Adults (Track the frequency of alleles across generations) - Gene pool: The total of all the eggs & sperms of a generation of one population - If the ending frequencies are different from starting frequencies, the population has evolved o Evolution resulting from blind luck “genetic drift”: Allele frequencies change somewhat across generations. o G. Udny Yule (1902): First biologist to trace the frequencies of Mendelian alleles across generations, but he concluded only 0.5 & 0.5 frequencies will result in equilibrium o Reginald Punnett: A population with allele frequencies that sums to 1 will remain unchanged  p + 2pq + q = 1  Evolution is a change in allele frequencies - The Hardy-Weinberg equilibrium principle: o The allele frequencies in a population will not change, generation after generation o If the allele frequencies in a population are given by p and q, the genotype frequencies will be given 2 2 by p , 2pq, and q  If both conclusions are true, the population is in Hardy-Weinberg equilibrium - Assumptions that cannot be violated for the Hardy-Weinberg equilibrium principle to be true (If violated, the allele frequencies of the population will change, the set of events that can cause evolution) o There is no selection, where all members survived at equal rates & contributed equal numbers of gametes to the gene pool o There is no mutation, alleles are not converted “mutated” into copies of other existing alleles, & no new alleles are created o There is no migration, no individuals moved into or out of the population o There are no chance events, or the model population is infinitely large, so individuals with different genotypes will pass on their alleles to the next generation equally o Individuals choose their mates at random, so there’s no mating preference for certain genotypes 6.2. Selection - Selection: Violation of the first assumption, individuals with particular phenotypes survive better or reproduce more than individuals with other phenotypes “reproductive success higher” o Leads to evolution if the phenotypes are heritable “associated with certain genotypes” o In nature, selection results in small, cumulative changes in allele frequencies - Drosophila melanogaster: o Experimental group with ethanol spiked in their food o Control group with normal, non-sFiked food o Over generations, the allele (Adh ) that contains the gene encoding the enzyme ADH (alcohol dehydrogenase) increased in the experimental group, with no changes in the control group o Adh homozygous encoded ADH breaks down ethanol 2x the rate compares to Adh homozygous - Genetic variation for resistance to kuru “fatal neurological disorder of the Fore people” o Kuru “uncontrollable shivering & trembling” (E.g. Bovine spongiform encephalopathy)  Belongs to a group of maladies known as the spongiform encephalopathies “brain looks like a sponge  degenerating tissues through the host’s production of mis-folded PrP proteins, unknown vector as of today” BIOL359 - Evolution Winter 2013  The genotype for PrP gene on chromosome 20 influences an individuals’ susceptibility to the disease  2 alleles @ position 129, 1 encodes for valine & other encodes for methionine  All victims of Kuru had Met/Met genotype (Homozygous diseased) not Met/Val or Val/Val  Statistically significant excess of heterozygotes & deficit of homozygotes  Homozygotes are susceptible to kuru and heterozygotes are resistant 6.3. Patterns of Selection: Testing Predictions of Population Genetic Theory - Selection on Recessive and Dominant Alleles o Flour beetles, heterozygote fonder, initial allele frequency of the 2 alleles are 0.5 & 0.5, homozygous recessive individuals have zero fitness  Over 12 generation, dramatic increase of the non-lethal dominant allele, rate of evolution is rapid at first, but slows down as the experiment proceeds o When a recessive allele is common, evolution by natural selection is rapid o When a recessive allele is rare & a dominant allele is common, evolution by natural selection is slow  Most are phenotypically hidden inside heterozygous individuals, immune from selection - Selection on Heterozygotes & Homozygotes o D. melanogaster, heterozygotes founders, initial allele frequency of the 2 alleles are 0.5 & 0.5, homozygous recessive individuals have zero fitness  Frequency of the viable allele increased rapidly over the first few generations, but rate of evolution slowed down & reached equilibrium at a frequency of 0.79 instead of 0.94 like the flour beetles example shown above o Heterozygote superiority/Overdominance: Heterozygotes have higher fitness than either homozygotes, at equilibrium, the selective advantage enjoyed by the lethal allele in heterozygotes balances the obvious disadvantage it suffers when it is in homozygotes  Maintenance of genetic diversity among populations o
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