In response to requests for more study questions than the old exams I have made available, you may wish to review these study questions for Exam 2
Freeman and Herron:
Chapter 4: 1, 2, 3, 4, 7, 8, 9a,b
Chapter 5: 1, 2, 3, 8
Chapter 6: 1, 3
Chapter 7: 1, 8, 9
Here are some other questions I found on the class webpages with links on our class page:
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Basic Hardy-Weinberg stuff:
1) What assumptions are made when modeling a population using Hardy-Weinberg?
2) Be able to prove that the frequency of the Aa genotype after one generation of random mating will be 2pq and the frequency of the aa genotype will be q squared.
3) Show how two (or more) populations with different genotype frequencies, but identical allele frequencies will equilibrate to identical genotype frequencies after
one generation.
4) Know examples (real or not) of populations that both exist in Hardy-Weinberg equilibrium and those that don't.
5) Though we have not gone over it in class, know the Hardy-Weinberg equation for one locus and two alleles.
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Multi-locus genetics:
1) What is the equation for Hardy-Weinberg equilibriim for one locus and three alleles?
2) List 4 ways that the effective population size can be different from the actual population size.
3) Define linkage.
4) Define haplotype.
5) Define 'D' (linkage).
6) Does the frequency of the haplotype A1B1 (a) decrease or increase when there is recombination between single or double homozygotes (at A and/or B)?
7) Does the frequency of the haplotype A1B1 decrease or increase when there is recombination between double heterozygotes?
8) By how much do these increase or decrease?
9) How is the equation a' = a-r(D) derived?
10) What does it say about the relation between the frequency of the A1B1 haplotype and linkage?
11) How is the equation D'= D (1-r) derived?
12) What does this say about linkage over time?
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Genetic Drift:
1) What is random sampling?
2) Define genetic drift.
3) Define founder's effect.
4) What is the probability that 'n' individuals taken from a population will all be homozygous?
5) In a population such as the one discussed in class, what is the probability that a gamete will combine with another from the same parent?
6) What is the probability that it will combine with a gamete other than that from the same parent?
7) What will the frequency of homozygous individuals be in a second generation? Of heterozygotes?
Here
are some questions from Joe Travis’ class at Florida State:
3.What do we mean when we speak of "hidden genetic variation" in the context of selection and evolution in polygenic traits?
17.What is the significance of homologies that are not analogies, and how might that significance be related to the idea that small changes in early development produce large differences among adult forms?
19.Consider our fish with the variable vertebral numbers again. We have a stock in which all fish have 18 vertebrae, and we know that we have only Ab and aB gametes in our stock.
a.Obviously D < 0 in our stock. Is the release of stored genetic variation possible only if D < 0 or can stored variation be released when D > 0?
b.If the two loci have a recombination fraction of 0.01, how many generations will it take before the absolute value of D is less than the recombination fraction?
c.We decide we like "mediocre" fish (with 18 vertebrae), and we will sterilize any fish that shows up in our colony with either more or fewer vertebrae. Will we have to check our stock every generation, or will there be a point at which we will no longer have to worry because it will be impossible (barring mutation) to get a fish with any number of vertebrae other than 18? Does your answer change as the recombination fraction between the loci changes?
d.Now let's assume we have a very large colony of fish with all vertebral numbers, that the two loci are indeed unlinked, and that D = 0. We still would rather have mediocre fish (with only 18 vertebrae), so we embark on our sterilization program again. After about five generations of this artificial selection, will D still be 0? If not, will it be positive or negative in sign?
e.Can you describe any way in which we could get a stock of fish in which most if not nearly all fish had 18 vertebrae but the colony had D > 0?
20.Let's look at the slug Mucosus nauseatus. There are three genotypes, and their mucus-secretion rates and relative frequencies are as follows:
A1A1 10 cc/day 0.64
A1A2 8 cc/day 0.16
A2A2 2 cc/day 0.20
a.Are the genotypes at the A locus at Hardy-Weinberg frequencies?
b.What is the genetic variance in mucus-secretion rate?
c.If the alleles at the A locus had the same frequencies as above but were at Hardy-Weinberg genotype frequencies, would the level of genetic variance be the same as, exceed, or be less than the level in our slug population?
21.Mutation rates are sufficiently low, per locus per gamete per generation, not to be a strong force in producing evolution. Yet a close personal friend of yours claims that in fact mutations are very common in natural populations and therefore mutation rates play a significant role in evolution. Resolve this paradox.
22.If the genotypes at two loci are each at Hardy-Weinberg equilibrium frequencies, can there be gametic disequilibrium between the loci? If two loci are in gametic equilibrium, can the genotypes not be in Hardy-Weinberg equilibrium?
23.Consider a population in which all males have the genotype "aa" and all females have the genotype "AA" at a diploid, autosomal locus. Males and females are equally common. How many generations will elapse before the Hardy-Weinberg equilibrium is reached at this locus if mating is random?
24.A critic of the role of population genetics in evolution once said that the discipline of population genetics was silly because all its practitioners thought of evolution as a process of replacing one bean with another, that is, all they cared about was exchanging one allele for another via gradual replacement, one locus at a time. Clearly this critic has misunderstood the role of population genetics. Why do we study changes in allele frequencies, and is it true that we only think about one locus at a time? Which phenomena require multilocus explanations?
25.An experimental population of barley (Hordeum vulgare) was established by intercrossing of 30 barley varieties from various parts of the world. Two loci (A and B) coding for esterases were examined at various times; two alleles (1 and 2) were present at each locus. The gametic frequencies in three different generations were as follows (several thousand gametes were examined in each generation):
Gamete Relative Frequencies
Generation A1B1 A1B2 A2B1 A2B2
4 0.354 0.256 0.387 0.003
14 0.407 0.098 0.491 0.004
26 0.453 0.076 0.452 0.019
a.Calculate the value of D for each of these three generations.
b.What process(es) is (are) likely to be responsible for changing the gametic disequilibrium as the generations proceed?
c.If these two loci were tightly linked, how would this linkage affect the change in D over generations?
26.Consider a population of sea urchins with the following relative frequencies of gamete genotypes at two loci:
Genotype Relative Frequency
A1B1 0.91
A1B2 0.00
A2B1 0.00
A2B2 0.09
a.Calculate the initial value of D.
b.Assuming random mating, what will the genotypic frequencies equal in the next generation after these gametes unite?
c.If there in no linkage between the two loci (r = 0.5), what will the value of D equal in the fifth generation?
d.If the two loci are linked and r = 0.2, what will the value of D equal in the fifth generation?
27.In Shorthorn cattle, the genotype A1A1 is phenotypically red coat color, A1A2 is roan (a mixture of red and white), and A2A2 is white.
a.If 108 red, 48 white, and 144 roan animals were found in a sample of Shorthorns from the central valley of California, calculate the frequencies of the A1 and A2 alleles for this population.
b.Is this population in Hardy-Weinberg equilibrium for the coat color locus? Prove your answer mathematically.
c.If this population is completely panmictic, what would be the expected genotypic frequencies of the next generation?
28.Consider the following phenotypic trait values for a single locus with two alleles:
Population A1A1 A1A2 A2A2
1 2.0 1.5 1.0
2 2.0 2.0 1.0
3 1.0 2.0 1.0
4 2.0 1.0 2.0
5 2.0 1.7 1.0
Each population represents an example of a different genetic relationship between the two alleles. The examples are complete dominance of A1, partial dominance of A1, no dominance, underdominance, and overdominance. Identify, in each population, which genetic relationship between the two alleles is described by the above trait values.
30.Most of the differences between maize and its wild progenitor, teosinte, can be attributed to the effects of only four genes. Nonetheless, these two plants have very different phenotypes. How might you resolve this paradox?
31.Mutations are clearly biased; certain specific mutations at a locus occur more often than others (e.g. pelage mutations in mammals). What might be the evolutionary significance of this phenomenon?
33.What do we mean, specifically, when we use the term "genotype-environment interaction"?
34.It is claimed that humans and chimpanzees share over 98% of their genes; nonetheless, these two species look remarkably different to me and have some very different physiological attributes. Can you resolve this paradox?
35.Consider the hypothesis that mutations occur randomly along the string of nucleotides within an exon in a eukaryotic gene. We would test this hypothesis, in principle, by examining the DNA sequences of descendents of a germ cell and performing some sort of statistical analysis on where the mutations occur. But suppose we could examine the DNA sequences only of zygotic cells and some mutations were lethal, which prevents us from even seeing those mutants (because their carriers never appear in our experimental group). Do these lethal mutants create a bias that impairs our ability to test the original
hypothesis?
36.One often reads about mutations being "random." In what sense are mutations random, and in what sense are they not?
37.Through which mechanisms do entirely new genes appear to arise? Did you read Chapter 4? Remember there are several--answering this question requires more effort than first appearances might suggest.
40.Let's play JeopardyTM. The answer is "Because mutations that are neutral in one generation or in one location can be beneficial or deleterious in another generation or location." What might the question be?