1.
Clearly explain what p and q represent in the Hardy-Weinberg equations. Write the equations, verbally describe the mathematical relationships among those variables, and explain the conditions under which those relationships hold.
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2.
Define heterozygote superiority and explain its effects on allele frequencies over time. Discuss Mukia and Burdick's test of this hypothesis. What important consequence(s) does this process have for the maintenance of genetic diversity over time?
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3.
Define the terms "population" and "gene pool" as they apply to population genetics. Given a population with two alleles (B and b) in which 30% of gametes receive the B allele and 70% receive the b allele, follow the population from this group of gametes, through fertilization and the formation of adults, to the production of the next generation of gametes. Assume that no "blind luck" is involved, and be sure to specify the frequencies of gametes and genotypes at the appropriate stages.
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4.
Define underdominance and describe Foster and colleague's experimental study of this phenomenon using Drosophila models. What is/are the general effects of underdominance on allele frequencies over time? Explain, in non-mathematical terms, why these results obtain. In what way are its effects similar to those of heterosis and in what way are they different?
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5.
Describe Cavener and Clegg's work on selection in Drosophila. What did they test, how did they test it, and what were their results? When selection acts, can we calculate genotype frequencies by multiplying allele frequencies? Explain.
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6.
Describe how Dawson tested the basic population genetics model for how populations should evolve when selection acts against recessive alleles. Although his recessive allele decreased in frequency, it wasn't eliminated from the population -- even though it was lethal in the homozygous condition. Why not?
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7.
Describe the mutation-selection balance model for the maintenance of deleterious alleles in populations. How can a mutation-selection balance hypothesis be tested? Use spinal muscular atrophy and cystic fibrosis to illustrate. What mechanism is most likely (given current evidence) to explain the relative abundance of deleterious CFTR alleles? Explain the evidence for this view.
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8.
Describe the reasoning used by U.S. geneticists to support compulsory sterilization to reduce the incidence of "feeblemindedness" in the United States. Explain, using Hardy-Weinberg principles, why this was a poor plan even from a "purely" evolutionary standpoint (i.e., without regard to basic principles of human rights). Extend this argument to explain why compulsory sterilization is an unworkable way to decrease the frequency of those human genetic diseases that are definitely known to be inherited as simple Mendelian recessive traits.
[Hint ]
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9.
Discuss how Matthijs and colleagues tested the hypothesis that some of the loss-of-function mutations in PPM2 are more severe than others.
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10.
Explain what is meant by the statement that the Hardy-Weinberg equilibrium equations are a null model.
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11.
Petal color in a hypothetical population of flowering plants is determined by a single gene with two co-dominant alleles. RR plants have red flowers, WW plants have white flowers, and RW plants have flowers with red and white striped petals. In a random sample of plants from this population you find 50 plants with red flowers, 20 with striped flowers, and 30 with white flowers. Caluclate the frequency of each genotype and of each allele. Is the population in Hardy-Weinberg equilibrium? Why or why not?
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12.
Under what condition(s) does selection lead to evolutionary change?
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13.
What is frequency-dependent selection? Discuss Gigord et al.'s studies on polymorphism in Elderflower orchids, and clearly explain how they supported the hypothesis that the balanced polymorphism in these flowers was the result of negative frequency-dependent selection. What are the general effects of this form of selection?
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14.
When the conditions of the Hardy-Weinberg equations are met, what happens to allele frequencies in populations over time? What happens to genotype frequencies? How can you test whether or not a population is in Hardy-Weinberg equilibrium?
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15.
Why is mutation considered to provide the raw material for evolutionary change? By itself, does mutation cause substantial evolutionary change? Why or why not? Using Lenski et al.'s work on E. coli to illustrate, explain how selection allows mutation to become a potent evolutionary force.
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16.
Will the current AIDS epidemic lead to an increase in the frequency of the CCR5 delta-32 allele within the near future (the next 100 years)? Why or why not (be sure to explain the evidence for your conclusion)?
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