For all of your answers EXPLAIN fully with examples as needed. 

REVIEW QUESTIONS - CHAPTER 1

  1. What is a retrovirus?  How are retroviruses similar to other kinds of viruses?  How do retroviruses differ from other kinds of viruses?
  2. How do retroviruses reproduce? Include all the steps in the life history of the HIV virus.
  3. How do viruses recognize which cells they have evolved to infect?  How do they attach to the host cell?
  4. What are the molecular and evolutionary significances of replication using reverse transcriptase rather than DNA polymerase? Explain why there are these differing results.
  5. How does HIV cause AIDS?
  6. See Figure 1.4.  Discuss what is happening to the CD4-T-cell count during the acute, chronic, and AIDS stages of an HIV infection.  Explain why.
  7. See Figure 1.4.  Discuss what is happening to the viral load during the acute, chronic, and AIDS stages of an HIV infection.  Explain why.
  8. How does AZT function as an antiAIDS drug?
  9. Why does AZT usually not interfere with normal cellular transcription (i.e. DNA to mRNA)? 
  10. Why could AZT potentially cause problems with replication?  Why is it unlikely that AZT could cause problems with transcription?
  11. Why do retroviruses such as HIV evolve resistance to drugs such as AZT so rapidly?
  12. Why does AZT fail in the long run? What mutations are responsible for this failure. In what molecule and where are these mutations expressed?
  13. Does AZT cause the mutations which result in HIV strains resistant to AZT?  If yes, explain how.  If no, explain how HIV becomes resistant.
  14. What is the "cost" to a population of HIV viruses that has evolved HIV resistance?  Why?
  15. In the presence of AZT, why are mutations for AZT resistance selected for?  Include a discussion of benefits and tradeoffs to the virus that  result from these mutations.
  16. Is evolution by natural selection unidirectional and irreversible? Why or why not?  Use evidence from the use/disuse of AZT to justify your answer.
  17. What is the advantage in having a high mutation rate in the gene that codes for reverse transcriptase?
  18. An HIV-positive patient takes AZT, but stops after his population of virions becomes resistant.  In the absence of AZT, why is there a back-mutation in the reverse transcriptase to original "wild" state of reverse transcriptase?  What is being selected for?  Include a discussion of benefits and tradeoffs to the virus in using the variants of RNA transcriptase.
  19. Explain figure 1.9.  What four evolutionary steps are involved?
  20. What is the evolutionary rationale behind Highly Active Anti-Retroviral Therapy (HAART)?
  21. Why are multidrug (HAART) therapies consisting of HIV protease inhibitors and reverse transcriptase inhibitors more successful than single drug therapies such as AZT in combating AIDS in persons infected with HIV?
  22. Why is HIV Fatal? Explain in terms of the proximate cause (how).
  23. Why is HIV Fatal? Explain in terms of the ultimate cause (why).
  24. Two biological constraints have been proposed to explain the high virulence of HIV. What is the evidence that the virulence is not caused by these two constraints.
  25. Why do retroviruses have much higher mutation rates than most nuclear genes?
  26. What is the advantage of having a high mutation rate in the gene that codes for reverse transcriptase?  What are the costs?
  27. Explain why there is a decrease in mutation accumulation as shown in Figure 1.10a.
  28. Evolution in HIV can be described as short-sighted.  Explain why.
  29. Two levels of selection can be ascribed to HIV evolution.  One is the evolution within the host.  The other is transmission between hosts.  What conflicts result from this?  What does this indicate about the nature of the evolutionary process.
  30. What is virulence?  What enables a pathogen to be highly lethal?
  31. What is the correlation between lethality and transmission of HIV?  What does this indicate about the best strategies in the fight against AIDS?
  32. From the second edition: Refer to Figure 1.5.  Using the transmission rate hypothesis, explain under which conditions high virulence strains of HIV will be selected for. Contrast this with the conditions in which high virulence will be selected against.  Discuss why the virus is more fit under the first set of conditions. What is the evidence that natural selection is favoring the high virulence strain in the first set of conditions versus the second?
  33. From the second edition: Why is high virulence of HIV selected for when there is a high rate of partner exchange?   Include a discussion of benefits and tradeoffs to the virus.
  34. From the second edition: Why is low virulence of HIV selected for when there is a low rate of partner exchange?   Include a discussion of benefits and tradeoffs to the virus.
  35. From the second edition: Refer to Figure 1.5.  Using the transmission rate hypothesis, explain under which conditions low virulence strains of HIV will be selected for. Contrast this with the conditions in which low virulence will be selected against.  Discuss why the virus is more fit under the first set of conditions. What is the evidence that natural selection is favoring the low virulence strain in the first set of conditions versus the second?
  36. From the second edition: Why is HIV-2 less virulent than HIV-1?
  37. From the second edition: The Ewald transmission rate hypothesis has not yet been shown to be the correct explanation for HIV (and other) virulence.   Explain why it is a scientific hypothesis.
  38. How does HIV enter cells?
  39. What is the molecular basis (CCR5-delta32) that causes some people to be resistant to infection by HIV?
  40. What is the evolutionary scenario that has been proposed to explain why some people are resistant to infection by HIV? Be sure to explain the role of natural selection in this process.
  41. What does HIV phylogeny show about how the virus has moved between host species. What does it indicate about the origin of AIDS?
  42. On figure 1.12, identify the nodes that represent the common ancestor of
    1. all human HIV-1 lineages and their chimpanzee SIV relatives.
    2. a group of SIV viruses that have not been transmitted to humans.
    3.  all human HIV viruses and all of their non-human primate relatives.
    4. one group of human HIV-1 viruses and their closest chimpanzee SIV relatives.
  43. From figure 1.12, what is the evidence that transmission of HIV from an SIV relative in non-human primates to humans has taken place multiple times?
  44. In Figure 1.12a,  HIV-1 is closer to SIVcpz and HIV-2 is closer to SIVstm. What does this imply about the evolutionary history of HIV? 
  45. In Figure 1.12a, HIV-1/U455 is closer to SIVcpz-US than it is to HIV-1/ANT70. What does this imply about the evolutionary history of HIV-1? 
  46. What is the difference between a drug and a vaccine?  How are each used in treating and/or combating infectious diseases?  Is AZT a drug or a vaccine?  Why?  What does it do that made it the first widely used treatment for people infected with HIV?  
  47. What is an epitope?  What is the advantage of having a high mutation rate in the genes that code for them?
  48. What is a vaccine? Explain the molecular basis of how they work.  Include a discussion of epitopes.
  49. What sort of vaccines are being developed against HIV?  What are the advantages of using a vaccine over using drugs to combat HIV?   Why are vaccines  likely to fail?  Include a discussion of epitopes.

REVIEW QUESTIONS--CHAPTER 2
  1. Define the following terms. Explain how each provides evidence for evolution. Discuss examples for each illustrating the process of evolution.
    1. Structural homology
    2. Embryological or Developmental homology
    3. Genetic homology 
    4. Analogy 
    5. Parsimony 
    6. Vestigial structure 
    7. Pseudogene 
    8. Processed pseudogene
    9. Direct observation of change through time 
    10. Fossil record 
    11. Transitional forms 
    12. Extinction 
    13. Law of succession 
    14. Geologic time scale 
    15. Radiometric dating
  2. What is microevolution?  What is macroevolution?  Are the two necessarily different from each other?  How are they similar?
  3. Explain what figure 2.1a shows.
  4. Explain what figure 2.1b shows.
  5. What was the evolutionary response of soapberry bugs to the introduction of flat-podded golden rain trees in Florida?
  6. What is the function of arrector pilli muscles?  Why do humans have them?
  7. How did Cuvier demonstrate the fact of extinction?  Why was this important in challenging the dominant European worldview of the time?
  8. How has the fossil record of the origin of birds provided evidence for evolution?
  9. How has the fossil record of the origin of whales provided evidence for evolution?
  10. What are phylogenetic trees?  Why did Darwin consider them so important?
  11. Explain why the bones in the forelimb of bats and birds are homologous, but bat wings and bird wings are analogous. 
  12. Give an example of a nonhomologous similarity.  Does this pose a problem for evolutionary biology?
  13. How do developmental homologies in the vertebrates provide evidence for evolution?
  14. Why is the genetic flaw illustrated in figure 2.16 better explained by evolution than by special creation.
  15. Referring to Figure 2.1, describe the pattern of change seen in soapberry bugs over time and its likely cause.   Frame your answer in terms of Darwin's Four Postulates discussed in Section 3.2, page 72.  Discuss what, if anything, on the figure supports each of the postulates.
  16. What is methodological naturalism?  How does it differ from ontological naturalism?
  17. Why is it necessary for a scientist to apply at least methodological naturalism, if not ontological naturalism, to the study of biological processes?
  18. FROM THE 3rd EDITION REVIEW QUESTIONS
    1. Briefly explain why shared "flaws", such as the presence of the proximal CMT1A repeat (SEE FIGURE 2.16), are particularly strong evidence in favor of descent with modification and against special creation.
    2. Compare and contrast Methodological and Ontological Naturalism. How is the adoption of Methodological Naturalism by science justified and how does it constrain the nature of scientific explanations? Is the Theory of Special Creation as outlined in the chapter introduction consistent with this approach to science? Why or why not? In theory, does the adoption of Methodological Naturalism imply disbelief in a divine creator? Why or why not?
  19. FROM THE 2nd EDITION REVIEW QUESTIONS (These also apply to the third edition!!)
    1. What is homology? Illustrate your answer with examples of structural, developmental, and genetic homologies. Explain how the presence of homologies supports the hypothesis of common ancestry rather than of special creation. 
    2. Describe the kind of distribution pattern Darwin found in animals of the Galapagos islands. Explain how this distribution supports the hypothesis of common ancestry rather than of special creation.
    3. What is a phylogenetic tree (i.e., what does it represent)?  
    4. What is a vestigial structure? Give examples of vestigial traits at the structural, developmental, and genetic level. Explain how the existence of these traits supports the hypothesis that organisms change over time rather than being fixed and immutable.
    5. Describe the pattern of change seen in soapberry bugs over time and its likely cause. What do these findings suggest about the Theory of Special Creation as it existed in Darwin's time?
    6. Discuss the fact of extinction, the law of succession in the fossil record, the nature and existence of transitional forms in the fossil record, and the evidence of environmental change over time, giving examples as appropriate. Explain how/why these support the hypothesis that organisms have changed over time. 
    7. Describe the principle of uniformitarianism. What is the geological time scale? What do the geological time scale, the geologic column, and the principle of uniformitarianism tell us about the age of the earth, and how does this argue against the Theory of Special Creation and in favor of the hypothesis of descent with modification?

Review questions -- CHAPTER 3
  1. Define the following terms. Explain, using examples, how each is involved in evolution.
    1. Darwinian fitness
    2. adaptation
    3. heritability
    4. reproductive potential
  2. Which of Darwin's four postulates do Figures 3.3a, b, and c demonstrate.  Explain.
  3. Why doe figure 3.3 demonstrate evolution?
  4. Why is beak shape an important attribute for an evolutionary biologist to study?
  5. Why are the Galapagos Islands such an excellent laboratory for evolution?
  6. Be sure to explain the figure completely. Thinking about how the Finch bill demonstrates Darwin's Four postulates,
    1. What does figure 3.6 demonstrate?
    2. What does figure 3.7 demonstrate?
    3. What does Figure 3.8 demonstrate?
    4. What does Figure 3.9 demonstrate?
    5. What does Figure 3.10 demonstrate?
  7. Why is the regression line 1978 above that of 1976 in Figure 3.7?
  8. Does Figure 3.8 demonstrate that the decline of the finch population in the 1977 drought was caused by the decline in seeds?  Assuming the answer is no, what is the explanation for the correspondence between the two?  Assuming the answer is yes, why isn't the correlation perfect?
  9. What is the role of reproductive potential in Figure 3.8a and 3.9?
  10. What do Figures 3.11 a, b, c demonstrate about the evolution of ground finches?
  11. What are the roles of individuals and populations in natural selection?
  12. What are the roles of phenotypes and genotypes in evolution?
  13. Discuss the back-mutation by AZT resistant strains of  HIV to the "wild state" in the absence of AZT as an example of "Selection is �backward-looking,' not �forward-looking'."
  14. Why can't evolution purposely produce adaptations that will be needed for future conditions?
  15. Discuss how evolution via "natural selection can produce new traits, even though it acts on existing traits."
  16. Can a trait arise "for the good of the species"? Explain using examples of how altruistic behavior evolves.
  17. Define and give examples of �preadaptation' and �exaption.' What do they indicate about the nature of the evolutionary process.
  18. Discuss the "panda's thumb" and the beak in Geospiza fortis.  Are these �perfect' adaptations?  Why do imperfect adaptations better evidence for evolution by natural selection instead of by special creation?
  19. Are evolutionary biologists using a tautology when they refer to �survivial of the fittest?'
  20. Creationists claim that the vertebrate eye is much to complex and involves so many dependent features to have evolved.  Why is this false?
  21. Why is using "Irreducible Complexity" to support special creation criticized as "an argument from credulity?"
  22. Explain how the example of gene co-option in Figure 3.17 supports evolution rather than special creation.
  23. Why is exaption important for evolution?
  24. END OF CHAPTER QUESTION 3
    1. Be sure to explain fully. Thinking about how the Finch bill demonstrates Darwin's postulates
      1. What would figure 3.6 have looked like if bill depth was not variable?
      2. What would Figure 3.10 look like if bill depth was variable, but the variation was not heritable?
      3. In Figure 3.7, why is the line from the 1978 data after the drought higher on the y axis than the line drawn from the 1976 data before the drought.
  25. FROM THE 3rd EDITION REVIEW QUESTIONS
    1. List and briefly explain each of Darwin's four postulates.
    2. Using beak shape in medium ground finches to illustrate, briefly explain the phrase "natural selection results in adaptation, not perfection."
    3. Describe the process of artificial selection as Darwin knew it and the process as specifically applied to the development of today's cultivated cauliflower. Be sure to include any relevant experimental evidence in your response.
    4. Describe how Jones and Reithel demonstrated Darwin's postulates and their outcome in an experimental snapdragon population. What aspects of their study were "natural"? Which were manipulated? Given what you know about living organisms, how well did their model system represent patterns likely to hold in nature?
    5. Using the medium ground finches of the Galapagos as an example, demonstrate that Darwin's postulates can be tested and verified in nature. Explain why these birds make a good model system for the study of natural selection.
    6. What, precisely, is the effect of selection on individuals? On populations? Does selection cause adaptive variation to arise? Explain.
    7. Explain the statement "Selection is backward-looking, not forward-looking."
    8. Explain how selection can produce new traits even though it can only act on existing variation, using examples from the text as appropriate.
    9. Can natural selection produce perfect adaptation? Why or why not? Use examples to support your answer. Why might evolution by natural selection be characterized as a random or chance process? In what sense is evolution non-random? Is evolution progressive? Justify your answer.
    10. Can a trait arise "for the good of the species"? Explain.
    11. Identify the three major problems that prevented the theory of natural selection from being widely accepted at the time it was initially proposed. Briefly explain the resolution of those problems. What is the Modern Synthesis, and how can Darwin's original postulates be restated in light of our understanding of modern genetics? 
    12. Describe Argument from Design as expressed by William Paley in Darwin's time and by Michael Behe in our own. Explain, in general terms, how random genetic mutation can lead to order, and how complex structures can evolve through the gradual Darwinian process of natural selection. What evidence do we have that Behe's views are incorrect?
  26. FROM THE 2nd EDITION REVIEW QUESTIONS (These also apply to the third edition!!)
    1. Outline the basic model of Darwinian natural selection, being sure to include mechanisms as appropriate.
    2. Define the terms "fitness" and "adaptation." Is fitness absolute? Explain.
    3. Using the medium ground finches of the Galapagos as an example (but including others as appropriate), demonstrate that Darwin's postulates can be tested and verified in nature. Explain why these birds make a good model system for the study of natural selection.
    4. Did natural selection occur in medium ground finches? Did evolution? Justify your answer.
    5. What, precisely, is the effect of selection on individuals? On populations? Does selection cause adaptive variation to arise? Explain.
    6. If selection acts on phenotypes, how does evolutionary change over time take place?
    7. Explain the statement "Selection is �backward-looking,' not �forward-looking'."
    8. In the absence of AZT, the AZT resistant allele for HIV reverse transcriptase is replaced by the "wild type" allele.  Why did this occur?   Include a discussion of "Selection is �backward-looking,' not �forward-looking'." 
    9. Explain how selection can produce new traits even though it can only act on existing variation.
    10. Can natural selection produce perfect adaptation? Why or why not? Use examples to support your answer.
    11. What is the "random" element in natural selection? In what sense is evolution non-random? Is evolution progressive? Justify your answer.

Review questions -- CHAPTER 4
  1. Define and discuss the importance of the following terms.
    1. point mutation
    2. synonymous substitution
    3. non-synonymous substitution
    4. loss-of-function mutation
    5. frameshift mutation
    6. jumping gene ("transposon") insertion
    7. gene duplication
    8. inversion
    9. ''supergene"
    10. linkage
    11. polyploidy
  2. How are new alleles created?
  3. What is the difference between a new allele and a new gene?  What is the significance of the difference?
  4. What is a point mutation?  Do all point mutations results in changes in protein function? Explain.
  5. What is the difference between a synonymous and non-synonymous point mutation?
  6. What is a neutral mutation?  
  7. What kind of mutation causes sickle cell anemia?  What are the effects of this mutation?
  8. What are loss of function mutations?  How are they used to determine mutation rate? 
  9. Why does use loss of function mutations to determine mutation rates give inaccurate results?  What is a better method?
  10. Why do humans have a higher estimated number of mutations per generation (Table 4.1) than mice?
  11. Discuss Denver et al.'s studies of the fitness effects of mutations on Caenorhabditis elegans. Why did the results for control ("normal" conditions) population differ from the results for the experimental population?
  12. Explain and discuss Figure 4.6a.
  13. What are the different results of mutation in a somatic cell and mutation in a germ cell?
  14. What is crossing over?  When, where, and why does it occur?
  15. Explain in full how unequal crossing over create new genes. Discuss, using examples, the three different possible outcomes in terms of functions that natural selection can use to modify these genes.
  16. What is the most common mechanism of gene duplication?  How can gene duplication result in the evolution of new genes and new proteins?
  17. How can overprinting produce new genes? Be specific in illustrating the mechanisms involved.
  18. How can reverse transcription produce new genes? What would be the best evidence that a gene originated by this mechanism? Cite an example.
  19. What are chromosome inversions? How do they promote tighter linkage? What is the evolutionary significance of tighter linkage. Use the example of clines in Drosophila (Figure 4.11) to illustrate your answer.
  20. Why is polyploidy much more common in plants than in animals?  How can polyploidization in plants result in the "instantaneous" formation of a new species?
  21. Discuss the methods that molecular geneticists use to determine the presence of different CCR5 alleles in populations.
  22. Calculate the frequency of the two CCR5 alleles for the British population in Table 4.4.
  23. Explain and discuss Figure 4.13.
  24. Explain and discuss Figure 4.14a.
  25. Explain and discuss Figure 4.14b.
  26. How is genetic variation determined?   Why does DNA sequencing show higher rates of genetic variation  than protein electrophoresis?

WEB SITE QUESTIONS: 1-12; http://cwx.prenhall.com/bookbind/pubbooks/freemanea2/

  1. Describe the basic structure of DNA, and briefly summarize the processes of replication, DNA repair, transcription, and translation.
  2. Explain why the genetic code is called a triplet code. What is a codon? In what way is the code redundant?
  3. Define the terms "gene," "locus," "allele," and "mutation." Illustrate your definitions with examples from human hemoglobin.
  4. What are point mutations?  What causes them, and what are the different kinds? Which are more common, transitions or transversions, and why? Discuss the effects of point mutations on fitness, using sickle-cell anemia to illustrate.
  5. What is a loss-of-function mutation, and how (in general) are they used to calculate mutation rates? Does using this type of mutation accurately estimate mutation rates? Why or why not?
  6. How common is mutation? Do mutation rates vary? If so, how, and why?
  7. How does gene duplication occur? Why is this phenomenon important evolutionarily? What evidence do we have that gene duplication has occurred? Illustrate using the globin gene family.
  8. How do chromosomal inversions occur, and what is their significance? Be sure to include a brief discussion of linkage.
  9. In what kind(s) of organisms is polyploidy common? How does it occur, and what is/are its evolutionary consequence(s)?
  10. Outline the mechanisms used to determine genotype. Given the appropriate data, explain how to calculate allele frequency. How much variation, in general, seems to exist in natural populations?
  11. Explain why the classic view assumed that genetic variation would be limited in natural populations? Briefly describe the two hypotheses for why natural populations are more variable than had been expected.
STUDY QUESTION FROM Kerry Kilburn, Old Dominion University
  1. Is all of the DNA in eukaryotic genomes used to build proteins? Explain. Briefly describe the structure of eukaryotic genes, being sure to define the terms intron and exon. What is mRNA processing?

Review questions -- CHAPTER 5
  1. Try solving these problems from Kansas State, Principles of Biology, Biology 108 
  2. More problems from North Harris College

More Problems

  1. If the dominant trait for being able to taste the chemical PTC (phenylthiocarbamide) is present in 60% of the population, what is the frequency of the recessive ALLELE (nontaster) in the population. What percent of the population are nontasters.
  2. Consider a stable population in which the recessive allele has a frequency of 0.8.  What percent of the population would be heterozygous?
  3. In a stable population, 91% of the individuals express the dominant phenotype.  What are the allele frequencies for the dominant and recessive alleles?  What percent of individuals expressing the dominant phenotype are homozygous?  (read this question carefully)
  4. In a population of 500 individuals, 200 are genotype AA, 125 are genotype Aa, and 175 are genotype aa.  What is the frequency of the dominant allele A?  What is the frequency of the recessive allele a?  Given these allele frequencies, what does Hardy-Weinberg predict will be the frequencies of each of the three genotypes?  Is the population in Hardy-Weinberg equilibrium?  Fully explain your answer.
  5. In a population of plants, there are white (A1A1), pink (A1A2), and red (A2A2) flowers. The genotype frequencies of these flowers are 0.16 white, 0.48 pink, and 0.36 red.  
    1. What are the allele frequencies for A1 and A2?
    2. Due to a decrease in the bee population the white flowers have lower relative fitness. w11 = 0.5. What are the new genotype frequencies?

  6. A certain population has p = 0.6 and q = 0.4 for the dominant and recessive alleles of a certain gene.  Assuming a stable population, what is the percentage of each genotype in the following generation?  If the fitness of the homozygous recessive phenotype = 0, what is the value of p and q and the percentage of each genotype in the following generation?
  7. For recessive alleles, the equilibrium frequency of that allele = q = (μ / s)1/2, where μ is the mutation rate and s is the selection coefficient against the recessive allele.
    1. 1/2000 of the people of northern Europe have cystic fibrosis (CF can be considered a recessive lethal allele).  If the population is in Hardy-Weinberg equilibrium, what is the frequency of the CF allele.  If this is the equilibrium frequency, what is the expected mutation rate.  If the actual mutation rate is 0.0000067, what conclusions can be drawn.  Why?
    2. If the mutation rate for the recessive sickle cell allele (lethal if homozygous) is 10-4, what is the expected percent of in individuals who are homozygous for this trait if it is established by mutation alone.  The actual frequency for individuals with this trait is 0.16. What is the most likely explanation for this?  Correctly use this formula [q = s1/(s1+s2)] to find the fitness of the homozygous dominant to support your answer. [s1 is the selection coefficient for the homozygous dominant and s2 is the selection coefficient for the homozygous recessive]
  8. In regions with malaria, individuals heterozygous for the recessive sickle cell allele have the highest fitness (w = 1), versus homozygous normals (w = 0.5), or homozygous recessives (w = 0).   Calculate the equilibrium frequencies expected for the three genotypes.  [q = s1/(s1+s2) ] 
  9. The scale eating fish shown in Figure 5.20 have a dominant "right-handed" allele frequency of  about 0.3.  Use Hardy-Weinberg to explain why this this is correct.

Review questions -- CHAPTER 5

  1. Define the terms "population" and "gene pool" as they apply to population genetics.
  2. What conditions must be satisfied to achieve Hardy-Weinberg equilibrium?   Why is the Hardy Weinberg model used in research in evolutionary biology?
  3. Why is the Hardy Weinberg model used in research in evolutionary biology?
  4. Referring to Figure 5.12, explain what is meant by "strong" and "weak" selection in terms of fitnesses of homozygous dominants, heterozygotes, and homozygous recessives.  Explain how the strength of selection influences the rate of evolution.
  5. Apply the reasoning developed in your answer to the previous question to the three HIV/CCR5delta32 scenarios in Figure 5.15.  What are the implications for evolution changing HIV resistance in Europe and Africa?  Why?
  6. Will the current AIDS epidemic lead to an increase in the frequency of the CCR5delta32 allele within the next 40 generations or so?   Discuss the three different scenarios presented in the text for high or low frequency of the allele and high or low infection and mortality rates.  Which of the three scenarios is required for this to happen?  Which one applies to western Europe?  to Africa?
  7. 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)?
  8. Explain the change in frequency of lethal recessive alleles over time as illustrated in Fig. 5.16.
  9. Why are rare alleles mostly in the heterozygous condition, and not the homozygous condition.  Use the equation for the Hardy Weinberg equilibrium to justify your answer.
  10. Discuss (and give examples of) the effects of selection of on allele frequencies when
    1. the dominant phenotype has a greater fitness than the recessive phenotype.
    2. the recessive phenotype has a greater fitness than the dominant phenotype.
    3. the heterozygotes have greater fitness than either of the homozygotes
    4. the heterozygotes have lower fitness than either of the homozygotes
  11. [FROM THE SECOND EDITION] What kind of selection do the scale eating fish (Figures 5.19 and 5.20) demonstrate?  Why doesn't one form (left-handed or right-handed fish) replace the other? 
  12. Fully explain why most sexually reproducing species have 50% males and 50% females.
  13. Discuss the significance of Fig. 5.25.  Why is mutation considered to provide the raw material for evolutionary change? By itself, does mutation cause substantial evolutionary change? Why or why not? Explain how selection allows mutation to become a potent evolutionary force.

Chapter 5 end of chapter questions

  1. In humans the COLA1A1 locus codes for a certain collagen protein found in bone. The normal allele at this locus is denoted with S. A recessive allele s is associated with reduced bone mineral density and increased fractures inn Ss and ss women. A recent study showed of 1778 women showed that 1194 were SS, 526 were Ss, and 58 were ss.
    1. What are the genotype frequencies?
    2. What are the allele frequencies?
    3. Are these two alleles in Hardy-Weinberg equilibrium? How do you know? 
    4. What information do you need to determine whether the alleles will be in equilibrium in the next generation?
    5.  Redo A-C with the following data: of 1278 women, 1194 were SS, 26 were Ss, and 58 were ss.

Chapter 5 web site questions

  1. Explain what is meant by the statement that the Hardy-Weinberg equilibrium equations are a null model.
  2. What, specifically, do the Hardy-Weinberg equations describe (be sure to explain any conditions that are assumed by the model)?
  3. Clearly explain what p and q represent in the Hardy-Weinberg equations. Write the equations and verbally describe the mathematical relationships among those variables and the conditions under which those relationships hold.
  4. Given genotype frequencies, be able to calculate allele frequencies. Given allele frequencies and assuming the conditions of Hardy-Weinberg are met, be able to calculate genotype frequencies.
  5. When the conditions of the Hardy-Weinberg equations are met, what happens to allele frequencies in populations over time? What happens to genotype frequencies?
  6. How can you test whether or not a population is in Hardy-Weinberg equilibrium? Given data in the form of genotype frequencies, be able to perform this test.
  7. Under what condition(s) does selection lead to evolutionary change?
  8. 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.
  9. Describe Dawson�s findings from his study of selection in Tribolium beetles. What was the "surprising" result of this study? Describe the mechanism responsible for this result and its general implication for selection acting on deleterious recessive traits.
  10. Briefly discuss the differences between selection acting on recessive alleles and selection acting on dominant alleles.
  11. Define heterozygote superiority and explain its effects on allele frequencies over time. Use sickle-cell anemia as an example in your explanation.
  12. Define heterozygote inferiority and explain its effects on allele frequencies over time. In what way are its effects similar to those of heterosis and in what way are they different?
  13. [SECOND EDITION] What is frequency-dependent selection? Discuss Hori�s studies on scale-eating fish, and clearly explain how he supported the hypothesis that the balanced polymorphism in these fish was the result of negative frequency-dependent selection. What are the general effects of this form of selection?
  14. What is frequency-dependent selection?  What are the general effects of this form of selection?
  15. 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.
  16. Why is mutation considered to provide the raw material for evolutionary change?  By itself, does mutation cause substantial evolutionary change?
  17. 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.
  18. 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.
  19. Describe how Dawson tested the basic population genetics model for how populations should evolve when selection acts against recessive alleles (his study of selection in Tribolium beetles, Fig. 5.16). 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?
  20. 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?

Chapter 6 - Review questions
  1. Define and give examples of each of the following.  Discuss the effect of each on Hardy-Weinberg equilibrium, genetic diversity, allele frequency, and evolution.  How does population size affect each?
    1. migration
    2. genetic drift
    3. genetic bottleneck
    4. founder effect
    5. inbreeding depression
  2. Discuss the interaction between selection, genetic drift, and mutation in small and large populations.
  3. Non-random mating can affect evolution.
    1. Define the coefficient of inbreeding.

    2. Define the term "inbreeding depression"

    3. Describe the conservation history of the greater prairie chicken in Illinois, and explain Westemeir et al.'s hypothesis for its decline even after reserves had been established and existing populations protected.
    4. Discuss how they tested their hypothesis and explain the results of those tests.
  4. Explain the role of migration in the banding patterns in island forms of the Lake Erie water snake.
  5. Even though banded snakes on islands in Lake Erie have a much lower fitness than unbanded snakes, they persist at much higher population levels than is predicted by selection.  Explain why this is so.  What would be expected to happen if selection were the only evolutionary force at work?
  6. Figures 6.06 and 6.07 shows color band variation in snakes on the mainland (two histograms on the left) and on nearby islands, increasing in distance from land. Category A snakes are unbanded, B and C intermediate, and D strongly banded. What is the explanation for this distribution of patterns (What are the two main evolutionary forces at work?).  Under what conditions would the island snakes be nearly all banded? nearly all unbanded?
  7. Using Figure 6.15, explain how population size affects genetic drift.
  8. Discuss the significance of Figure 6.16.
  9. What observations on the molecular evolution of the influenza virus provides evidence for the neutral theory of evolution?
  10. Discuss the factors responsible for the pattern of genetic variation seen in populations of collared lizards in the Ozarks (Fig. 6.18)
  11. Discuss the interactions of genetic drift and selection on mutations of different fitness from a neutral and a selectionist point of view.
  12. If a replacement mutation is disadvantageous, will drift or selection have a greater effect on the frequency of the allele for the mutation in the population? Explain
  13. Define and give examples of the founder effect. Discuss its effect on Hardy-Weinberg equilibrium, genetic diversity, allele frequency, and evolution.
  14. What is inbreeding and what is its effect on allele and genotype frequencies?
  15. What is the probability that the offspring of the half siblings below will inherit two copies of the same allele. What about the offspring of full siblings?
  16. Discuss the effects of nonrandom mating genotype frequency and on allele frequency? Specifically demonstrate changing genotype frequencies over five generations of selfing. Give several actual examples of the evolutionary consequences of non-random mating.
  17. What is the evidence for inbreeding depression in humans? Draw a graph that illustrates this effect.
  18. How have habitat destruction, deleterious alleles, genetic drift, inbreeding depression, migration, and nonrandom breeding affected the population genetics of the greater prairie chicken?
  19. Why was the Illinois Greater Prairie Chicken experiencing a "mutational meltdown"?
  20. Why did the introduction of outside migrants potentially rescue the Illinois Greater Prairie Chicken?

Chapter 6 end of chapter questions.

  1. Gene frequencies in small populations can change at different rates than in large populations.  State whether and explain why the following processes will typically have smaller, greater, or similar effects on evolution in small versus large populations.
    1. Migration

    2. Genetic drift

    3. Inbreeding

    4. New mutations per individual

    5. New mutations per generation in the whole population

    6. Substitution of a new mutation for an old allele

    7. Fixation of a new mutation

    8. Selection

Chapter 6 - Web Site questions

  1. Define migration in the context of evolutionary biology. Describe the one-island model of migration, and explain its key predicted outcome.
  2. Explain the role of selection and migration in the maintenance of polymorphism in banding patterns in island forms of the Lake Erie water snake. Be sure to discuss what pattern would be expected if either process were operating without the other. 
  3. Define the term "genetic drift," and give a verbal explanation of this process. Defend the argument that genetic drift results in evolutionary change but not in adaptive change. When drift operates, which of the assumptions of the Hardy-Weinberg equilibrium principle has been violated?  What is the general relationship between the effect of drift and population size? 
  4. Describe Giles and Goudet's study of red bladder campion and the effects of migration on genetic diversity in these plants. Be sure to explain the natural history of their study site and the way(s) in which this created a good model system for the study of migration. What predictions did they make, and how did they test them? What were their key findings?
  5. Explain the founder effect using relevant examples.
  6. Explain the founder effect using Clegg et al.'s work on genetic diversity in Australian/Tasmanian silvereyes and the frequency of achromatopsia in the Pingepalese people to illustrate. For Clegg et al.'s work, clearly describe the model system they used, the predictions they made, and how they tested the predictions 
  7. If drift is allowed to continue over many generations, what changes are predicted in allele frequency and heterozygosity? Illustrate these patterns using Buri's experimental study of fruit flies, Templeton et al.'s studies of Ozark collared lizards, and Young et al.'s plant studies. 
  8. When genetic drift is the only mechanism of evolution operating, what is the relationship between the rate of evolution, the rate of substitution, and the mutation rate? Under drift, how does population size affect the generation and maintenance of genetic diversity? Briefly describe the two general schools of thought on how important an evolutionary force neutral mutation is. 
  9. Briefly describe the neutral theory of molecular evolution. What initial observations caused Kimura and others to conceive of the theory? What predictions does it make, and how have those predictions been tested. Have the predictions been met?
  10. Explain the basic approach by which investigators use the neutral theory as a null model to test whether or not natural selection has caused molecular evolution.  In what kinds of loci does natural selection seem to play a particularly strong role?
  11. What is inbreeding and what is its effect on allele and genotype frequencies? Does inbreeding cause evolutionary change? Why or why not? 
  12. Explain Hamilton's reasoning for predicting that inbreeding may be common in the malaria parasite, and describe Paul et al.'s tests of this hypothesis. 
  13. Define the coefficient of inbreeding. If F is greater than zero, what does that tell you about the frequency of heterozygotes vs. the frequency of homozygotes? Briefly describe how pedigree analysis can be used to calculate F. 
  14. Define the term "inbreeding depression" and illustrate using human infant mortality and reduction in hatching success in great tits. What broad patterns have been revealed about inbreeding depression through experimental studies on angiosperms? 
  15. Describe the conservation history of the greater prairie chicken in Illinois, and explain Westemeir et al.'s hypothesis for its decline even after reserves had been established and existing populations protected. Discuss how they tested their hypothesis and explain the results of those tests. Is the scenario presented by this species likely to be unusual for endangered species generally, or are the causes of its decline likely to apply to a number of species? Explain.

Chapter 7

  1. What is meant by a pair of linked loci?
  2. What is a haplotype?
  3. What are recombinant chromosomes how are they produced?
  4. How can recombinant chromosomes be used to map loci on chromosomes?
  5. What is linkage disequilibrium?  How is it measured?
  6. If a population is in linkage equilibrium and F(allele A) = 0.8, F(allele a) = 0.2, F(allele B) = 0.6, and F(allele b) = 0.4, 
    1. What is the expected frequency of the four haplotypes (Fig. 7.2a)?
    2. What is the expected frequency of the 16 genotypes (Fig. 7.3a)?
  7. How does sexual reproduction reduce linkage disequilibrium?
  8. Fully explain Figure 7.6.
    1. Why doesn't the value of D change when r = 0?
    2. Why does the value of D change most rapidly when r = 1?
    3. Why does the value of D change most slowly when r = 0.01?
  9. Fully explain Figure 7.7.
  10. How are nearby neutral markers (Figs. 7.11, 7.12) used to estimate the age of the CCR5-delta 32 allele?
  11. Why does Figure 7.11a indicate the GAAT and AFMB loci are close to linkage equilibrium?
  12. Why does Figure 7.11b and c indicate the CCR5 loci are in linkage disequilibrium with the GAAT and AFMB loci?
  13. Which  GAAT and AFMB alleles does the CCR5 delta 32 allele usually occur with?  Explain why this is so and discuss its historical significance.
  14. Discuss the significance of Fig. 7.11 in terms of linkage disequilibrium, genetic drift, selection, and the evolutionary history of the mutation (CCR5-delta 32) that confers resistance to the HIV virus.
  15. Maynard Smith made two assumptions in his null model to compare asexual versus asexual reproduction.
    1. Assumption one concerns number of offspring produced.  Discuss and evaluate this assumption in asexually and sexually reproducing populations.
    2. Assumption two concerns survival of offspring.  Discuss and evaluate this assumption in asexually and sexually reproducing populations.
  16. What are the advantages of asexual reproduction.  Explain the significance of Figure 7.17 in terms of this.
  17. Why does asexual reproduction give a reproductive advantage?  Give a numerical example to illustrate the reproductive advantage.
  18. What are the disadvantages of sexual reproduction?
  19. In Dunbrack et al.�s experiment with Tribolium (Fig. 7.18), explain
    1. how were the asexually evolving populations simulated?  Is this a reasonable way to do this?
    2. when the simulated asexual populations would have an advantage over the sexual populations.
    3. when sexually reproducing populations have an advantage over asexually reproducing populations.
    4. why the sexual populations out-competed simulated asexual populations.
  20. What are the advantages of asexual reproduction.  Explain the significance of Figure 7.18b and d in terms of this.
  21. What are the advantages of sexual reproduction. Explain the significance of Figure 7.18a and c in terms of this.
  22. Figure 7.20 illustrates Muller's ratchet. 
    1. Describe how Muller�s ratchet increases the number of deleterious mutations
    2. What are the roles of mutation and drift in Muller's ratchet
    3. Explain why drift tends to eliminate the classes with the fewest numbers of deleterious mutations, but not the classes with the highest
    4. How do drift and mutation increase genetic load?
    5. How does sex stop Muller's ratchet?
    6. In light of the Muller's ratchet model, what is the selective advantage of sexual reproduction?
  23. Explain how Mueller's ratchet (Fig. 7.20) can explain the results of Andersson and Hughes' experiment (figure 7.21).
  24. How do periodic bottlenecks in bacteria (Fig. 7.20) demonstrate Muller's ratchet?  What caused some of the bacterial populations to develop decreased fitness?
  25. Why are the shortcomings of Mueller�s ratchet as an explanation for the evolution of sexual reproduction.
  26. What is the Red Queen hypothesis?
  27. How does the Red Queen hypothesis explain the evolution of sexual reproduction?
  28. What is the evidence that sex is an adaptation to short-term change?
  29. Discuss figure 7.22.   How  does a host parasite arms race make sex beneficial?
  30. How does the study on New Zealand snails (Fig. 7.23) support the host parasite arms race hypothesis for the evolution and maintenance of sexual reproduction?
  31. In Lively�s study of New Zealand snail populations (Fig. 7.23), why are males less common in populations with low parasite infection rates?
  32. In Lively�s study of New Zealand snail populations (Fig. 7.23), why are males more common in populations with high parasite infection rates?

Web Site Questions

  1. Briefly describe (verbally and graphically) the phenomenon of genetic linkage. Define the term "haplotype." Use a numerical/graphical example to illustrate why, when we consider multiple loci, we can't necessarily accurately describe the genetic structure of populations by knowing only allele frequencies.
  2. Describe the phenomena of linkage equilibrium and linkage disequilibrium (being sure to accurately define each term). What conditions are true of loci if and only if they are in linkage equilibrium? What mechanisms can create linkage disequilibrium in random-mating populations? What eliminates linkage disequilibrium from a population?
  3. Can selection at one locus cause a change in allele frequency at another locus? Under what condition(s) can this occur? Are these conditions likely to be met frequently in nature? Defend your answer using Huttley et al.'s work on the human genome and Miyashita et al.'s work on Arabidopsis.
  4. Using the CCR5 locus as your example, explain how patterns of linkage disequilibrium can help investigators reconstruct the evolutionary history of genes and populations.
  5. Define the term parthenogenesis, and give examples of organisms capable of both sexual and asexual reproduction. Describe the paradox for evolutionary theory presented by Maynard Smith's null model for the relative advantages of sexual and asexual reproduction. Be sure to explain the null model itself, including its assumptions.
  6. Describe the experimental and theoretical work addressing the assumptions of Maynard Smith's model. What general conclusion can be drawn about those assumptions?
  7. Describe Muller's ratchet and explain the general phenomenon it attempts to describe. In light of this model, what is the selective advantage of sexual reproduction? Discuss the experimental work on Salmonella and endosymbiotic bacteria described in the text; were the results consistent with Muller's ratchet?
  8. Discuss the logic behind investigations into short-term benefits of sexual reproduction. That is, why does the hypothesis that drift causes linkage disequilibrium and sex restores it fail to be persuasive in and of itself? Describe the changing-environment model for the advantage of sexual reproduction, and outline experimental work that supports this model.
  9. Describe the basic reasoning behind "changing environment" models for the benefit of sexual reproduction, with special attention to how selection on multilocus genotypes creates linkage disequilibrium and why selection would favor mechanisms to reduce linkage disequilibrium. Describe the specific "Red Queen" hypothesis and discuss Lively's test of the hypothesis

Chapter 8 in the third edition

  1. What is a qualitative trait?
  2. What are quantitative traits?  What is distinct about their phenotypic expression?  Why?
  3. What determines height in humans?  Why has the average human height in the US increased 8 cm over the past 100 years?
  4. How can Mendelian genetics explain quantitative traits (Fig. 8.2)?
  5. If a trait is controlled by one locus, how many genotypes and phenotypes can their be?  two loci?  three loci?
  6. How is narrow-sense heritability measured?
  7. Discuss the information in figures 8.11a, b, ,c, and d.  What can you conclude from each one?  Why?
  8. What does figure 8.11d show?  Is this sufficient evidence for heritability of body size?  Ideally what if any further experiments would you like to conduct? Why?
  9. What is a cross-fostering experiment?  What is its purpose?
  10. Full explain Figure 8.12. 
    1. What does the top graph indicate about heritability?  Why?
    2. What does the bottom graph indicate about heritability?  Why?
    3. Is this sufficient evidence that heritability fully explains beak size in this bird species?  Why? 
    4. Which other explanation is possible for this correlation?
    5. Which experiment would allow you to decide whether body size is inherited in this species?
  11. How is heritability in humans estimated from twin studies?
  12. What is meant by response to selection (R)?  Explain the equation R = h2S.
  13. What can hereditability be used to determine?  What cant it be used to determine?
  14. What is a selection differential?  In figure 8.15a, determine the selection differential.
  15. Alpine Skypilots:
    1. Discuss the significance of the following three figures (8.20, 8.21, 8.22) in terms of heritability, selection differential, selection gradient, and response to selection (define and explain these 4 terms). What do they demonstrate about being able to predict the effects of selection.
    2. What was Galen determining in fig 8.20?  Why was it important that she determine this value?
    3. How did Galen measure the strength of selection (selection gradient) by pollinating bees?
    4. How did Galen determine relative fitness of flowers?
    5. What does it mean that selection differential (S) determined by Galen is 5%?
    6. What does it mean that response to selection (R) determined by Galen is 5%?
  16. What are the three modes of selection?  How does each affect the average value and variation of the character being studied?
  17. How does directional selection differ from stabilizing selection?  from disruptive selection? How does disruptive differ from stabilizing?
  18. Give examples of the three modes of selection.
  19. Why is it expected that most of the time stabilizing selection should be the most common?
  20. Why is there stabilizing selection on human birth weigth?
  21. Discuss and explain the selection factors at work and their results on the gall-making fly (Figure 8.24).
  22. Discuss and explain the selection factors at work and their results on the black-bellied seed cracker (Figure 8.25)
  23. What causes a trait to have high heritability?  In Fig. 8.26, both populations have the same heritability for height.  Why? What does this experiment tell us about attributing genetic causes to differences between populations?
  24. What does heritibility tell us about genetic differences between populations?  Why?
  25. What does heritibility tell us about differences within populations?  Why?
  26. Figure 8.27 is adapted from Murray and Herrnstein's book on IQ and ethnicity. Discuss why the argument derived from these figures (the genetic component of intelligence is affected by race) is erroneous, fallacious, and non-scientific.  
  27. Why did Murray and Hernstein conclude that difference in IQ between African Americans and European Americans is due to genetic differences and not environmental differences between the two groups?  Why did they minimize the environmental contribution?  Was this a correct assumption?  Why?
  28. What experiments would have to be done to test Murray and Hernstein's hypothesis?  What problems would there be in evaluating the results of these experiments?
  29. Describe and discuss the classic studies on yarrow (Achillea) by Clausen, Keck, and Hiesey.  What conclusions can be drawn concerning the roles of environment and genetics? (Fig. 8.29)
  30. Under what conditions do high altitude yarrow plants make more stems than low altitude plants?  Why?
  31. Which population of yarrow plants was best adapted to making a large number of stems?
  32. Discuss how the experiment on what controls the number of stems in yarrow plants (Fig. 8.29).  Fully explain which population is better at making more stems.   Give specific examples from the yarrow plants and discuss how these invalidate Murray and Hernstein's conclusions.
Website questions chapter 8: 3rd edition
  1. Define "heritability," clearly explaining what this quantity does and does not measure. Describe the relationship among heritability, phenotypic variation, genetic variation, and environmental variation.
  2. How is narrow-sense heritability measured? Under what condition(s) is this method valid? Use Smith and Dhondt's study of heritability in beak size in song sparrows to illustrate. Can heritability be measured for traits that are universal within populations? If not, does that mean that such traits are without a genetic component? Explain.
  3. Explain the conceptual relationship between measuring differences in fitness and measuring the strength of selection. Describe how to calculate the selection differential and the selection gradient. Is one of these two measures preferred over the other? Why or why not? Justify your answer using the Grants' study of beak size in Galapagos finches as an example (and be sure to address the important findings of that work).
  4. Describe the conceptual basis of the response to selection (R). In biological (rather than mathematical) terms, explain its relationship to heritability and selection differential.
  5. Describe Galen's experimental studies of selection on flower size in alpine skypilots. Be sure to clearly identify the hypotheses she tested and the ways in which her experiments allowed her to use the techniques of quantitative genetics. What were her findings and conclusions?
  6. Discuss the key flaws in Herrnstein and Murray's claim (in The Bell Curve) that differences in IQ between African Americans and European Americans is due to genetic differences between the two groups. Be sure to address the utility (or lack thereof) of using heritability to understand differences among populations. Ideally, what kind(s) of experiments could we do to test Murray and Herrnstein's claim directly? What kinds of outcomes might such experiments produce, based on work with other organisms?
  7. Define the term "mode of selection." For each major mode of selection, describe the "direction" of selection, the relationship between fitness and values of the trait in question, and how the mean value and variance of the trait will change over time. Be sure you can identify each of these patterns graphically, and give at least one good example of each.
  8. What is the "evolutionary puzzle" presented by the assumption that directional and stabilizing selection are the most common modes of selection? How is that puzzle resolved?

Chapter 9 Adaptation

  1. What is the adaptationist program?
  2. What are Gould and Lewontin's objections to the adaptationist program?  Why do male mammals (including humans) have nipples?
  3. Concerning neck length in giraffes.
    1. What is the Lamarckian explanation for the long necks?
    2. What has been the traditional explanation as an example of natural selection?
    3. Even if this explanation is correct, what evidence is there that adaptations are not necessarily ideal solutions?
    4. What direct evidence indicates that this is not the correct explanation?
    5. What is the current preferred hypothesis?
    6. What evidence of male giraffe behavior supports this hypothesis?
    7. What evidence of female giraffe behavior supports this hypothesis?
  4. Briefly discuss three alternative explanations other than selection concerning traits.
    1. Why can populations differ with respect to traits?
    2. Because a trait permits a specific function, is that necessarily why it evolved?
    3. Do traits indicate intelligent design?
  5. Discuss the significance of wing waving in tephritid flies [Figs. 9.5 and 9.6] as an excellent study of adaptation.  
    1. What three hypotheses were tested in this experiment?
    2. Discuss the experimental and control groups used and the significance of each.
    3. What experiment was done to show that both patterned wings and wing waving are necessary to intimidate jumping spiders?
    4. What were the predictions that were tested for each of the three hypotheses.  How could the results be used to confirm one of the three hypotheses?
    5. What were the results of the actual experiments done to test the hypotheses?
    6. How did this intimidation behavior likely evolve?
  6. Lizards and snakes were used as examples of observational studies of adaptation [Figs 9.8, 9.9, 9.10].  
    1. Define behavioral thermoregulation.
    2. Discuss the significance of thermal performance curves.
    3. What is the evidence that iguanas behaviorally thermoregulate?
    4. Why might this thermoregulation in iguanas not be adaptive?
    5. Discuss thermoregulation in garter snakes
      1. What observations suggest that garter snakes behaviorally thermal regulate?
      2. What was the experiment that indicates this behavior is adaptive.
      3. What is expected to happen to snakes under thin rocks?  medium rocks?  thick rocks?
      4. Discuss the results of table 9.2.
  7. In comparative evolutionary studies, such as the evolution of testes size in fruit bats, why is necessary to take the evolutionary history of the species being studied under consideration?
  8. The comparative method can also be used to study adaptation.
    1. What is the hypothesis about testis mass in fruit bats?  Why is this a reasonable hypothesis?
    2. What is the importance of using relative testis mass in evaluating this hypothesis?
    3. What were the results of Hosken's investigation [Fig. 9.11]?  What conclusions can be drawn from this?
    4. Why is it important that such studies incorporate the effects of phylogeny?
    5. When phylogeny is incorporated [Fig. 9.14], does this change the conclusions?  Explain.
  9. What does figure 9.12a purport to show?  What does figure 9.12b show?  What is the significance of figure 9.12c?   Discuss the significance of this figure to comparative studies of adaptation.  
  10. What does Figure 9.11b purport to show?  Figure 9.14b?  What is the difference between the two?
  11. [Omit]What is meant by phenotypic plasticity?  Discuss the experiment using water fleas (Daphnia) to demonstrate this phenomenon.
  12. [OMIT] Discuss the evolutionary principles involved in the evolution of the mammalian middle ear.
  13. Regarding selection on female flower size in Begonia involucrata [Fig. 9.19]
    1. Compare male and female flowers.
    2. What are the two hypotheses that were tested. 
    3. What was the mode of selection predicted for each?
    4. What were the results of the experiments?
    5. Which hypothesis do the experiments support?
    6. Why are these results not in accord with what is actually observed?
    7. If large size is adaptive, why are female flowers of this species not any larger than they are?
    8. Is this an example of evolutionary tradeoffs or evolutionary constraints?  Explain.
    9. Why does there have to be a tradeoff? 
  14. Fuchsia excorticata exhibits a trait that is apparently maladaptive: it maintains flowers on the plant after they lose the ability to produce or receive pollen.  Since fitness would be increased by dropping the flowers soon after they ceased to be functional, why hasn't natural selection evolved this trait?
  15. Regarding selection on flower color change in Fuchsia excorticata [Fig. 9.20]
    1. Explain what figure 9.20b shows.
    2. What two hypotheses are tested to explain why flowers change from green to red.
    3. Which hypothesis is rejected?  Why?
    4. Which hypothesis is accepted? 
    5. Why do the flowers change color from green to red?
    6. Why does it take 11 days for the flower to abscise?
    7. Is this an example of evolutionary tradeoffs or evolutionary constraints?  Explain.

Web Site Questions

  1. What is the "classic" hypothesis for the adaptive value of long necks in giraffes? Discuss the evidence that this hypothesis is incorrect, framing that evidence in terms of specific predictions and tests of those predictions. What caveats must be kept in mind when studying adaptation?
  2. Using the observational evidence from the text, evaluate the hypothesis that garter snakes make adaptive choices when looking for nighttime retreats. Be sure to frame your discussion in terms of the general hypothesis, its logical alternatives, the specific predictions derived from the hypothesis, and the observations used to test those predictions. Can you think of alternative, non-adaptive hypotheses that are consistent with the available evidence? If so, what tests could you perform to distinguish between the alternative hypotheses?
  3. What, in general terms, is "the comparative method"? Why, in general terms, is knowing the evolutionary relationships among species used in comparative studies necessary? Illustrate your answer using Hosken�s study of testes size in flying foxes.

Questions from Dr. Kilburn's webpage

  1. What is "naive adaptationism"? How can it best be avoided?
  2. Why are experiments particularly powerful tools in science? What are their disadvantages, if any? Use the example of Greene et al.'s study of wing markings and wing waving in tephritid flies to illustrate the major aspects of good experimental design. Be sure your explanation includes a clear statement of the hypotheses and predictions that were tested and the conclusions the investigators drew from their experimental work.
  3. What is the fundamental difference between experimental and observational studies? Use Simmons and Scheepers' observational study of neck length in giraffes to illustrate how observation can be used to derive and test hypotheses about adaptation.
  4. Using the observational evidence from the text, evaluate the hypothesis that garter snakes make adaptive choices when looking for nighttime retreats. Be sure to frame your discussion in terms of the general hypothesis, its logical alternatives, the specific predictions derived from the hypothesis, and the observations used to test those predictions. Hint: Think of the data on the thermal properties of different refugia (burrows, thin rocks, etc.) as part of the background data/information used to make specific predictions.
  5. Using the data on flower size and pollination in Begonia involucrata and flower color change in Fuchsia excorticata as examples, explain the role of trade-offs and constraints in evolution. What general implications do these studies have for the study of adaptation?

Question (modified) from Dr. Dianne Byers, Illinois State University

  1. In a comparative analysis, such as testes size in fruit bats, why is it necessary to take the evolutionary history of the species under study into consideration?

Chapter 10 -- Sexual Selection

  1. Define, give examples of, and explain the evolutionary significance of
    1. sexual dimorphism
    2. sexual selection
    3. relative parental investment
    4. intersexual competition
    5. male-male competition
    6. intrasexual competition
    7. female choice
    8. sperm competition
  2. Why can't sexual dimorphism be explained by natural selection?
  3. Why is sexual dimorphism a puzzle for evolutionary biologists?  Give examples.
  4. How do selection pressures on females usually differ from those on males?  What fundamental asymmetry does this lead to? 
  5. Describe the experiment used by Gage to demonstrate sperm competition and ejaculate size in fruit flies.
  6. What selection mode controls survival rates in marine iguanas?  What size iguanas have the highest survival rates?  Why?  How do the body masses of male and female iguanas conform to the predictions based on natural selection?  What accounts for any differences?
  7. Explain the roles of natural selection and sexual selection in determining body size in marine iguanas (Fig. 10.8a).
  8. When and why can alternative mating strategies in male coho salmon be successful?
  9. How has female choice affected evolution of male barn swallows? Discuss the experimental evidence that female choice drives sexual selection.  How do male barn swallows benefit from this?  Are there costs to the males?  How do female barn swallows benefit?  What is the experimental evidence for this?  How do females that pair with less desirable males increase their fitness?
  10. How has female choice affected evolution of behavior in male green tree frogs? Discuss the experimental evidence that female choice drives this.  How do male green tree frogs benefit from this?  Are there costs to the males?  How do female green tree frogs benefit?  What is the experimental evidence for this?
  11. Discuss courtship and mating in hangingflies.  How do the males and females benefit from this behavior?
  12. Pipefish were cited as an example of an exception that can prove the rules of sexual selection.  Fully explain why.
  13. How can sexual selection explain why humans are sexually dimorphic?  Give examples.

Web Site Questions

  1. Define and give examples of sexual dimorphism. Does it occur in humans? Explain. Why is sexual dimorphism a puzzle for evolutionary biologists? How did Darwin begin to solve the puzzle?
  2. Defend the argument that sexual reproduction creates different selection pressures for males than for females. Be sure to clearly outline the logic behind the argument and state its fundamental prediction. Then, use Bateman�s studies of reproductive success in
    fruit flies to show how this prediction can be tested and what the results of those tests were.
  3. What specific differences in mating behavior between males and females are predicted by the presence of asymmetry in the factors limiting reproductive success for each sex? How, in general, will those differences be manifested? Under what general conditions might we
    expect a different pattern?
  4. In what general ways does sexual selection by male-male competition occur? On what grounds did Wikelski and colleagues suspect that sexual size dimorphism in marine iguanas was the result of sexual selection for large body size in males? How did they test this hypothesis, and what were their results? If sexual selection for large body size occurs in a species, can small males still achieve some mating success? How?
  5. Under what conditions might sperm competition be an important form of male-male competition? Describe the tests Gage used to demonstrate sperm competition via ejaculate size in Mediterranean fruit flies. Other than increasing ejaculate, what traits might be selectively advantageous for males subject to sperm competition?
  6. Discuss the system of infanticide in African lions, explaining how this can be considered a form of male-male competition. Explain why spontaneous abortion by females following pride take-over is an adaptive strategy.
  7. What initial observations suggested that sexual selection was operating in barn swallows and gray tree frogs? Describe how investigators tested the hypothesis that females practice active mate choice in these species. On what characteristics did females base their selection? In the case of barn swallows, what specific benefits did the "selected" males obtain?
  8. Describe the two general ways females are thought to benefit directly from exercising mate choice. Using evidence from gray tree frogs and hangingflies to illustrate your answer.

Questions from Dr. Kilburn's webpage

  1. Describe the "puzzle of sexual dimorphism" and explain how, in general terms, Darwin solved it. Defend the statement that sexual selection is simply a special case of natural selection rather than a separate process.
  2. Explain how asymmetries in reproductive investment set the stage for sexual selection. In general, which sex makes the greatest reproductive investment? In general, what two forms does sexual selection take (and why)?  What are the general exceptions to these "rules"?
  3. Under what conditions might we expect male-male competition to be an important form of sexual selection? Describe Wikelski et al.'s studies of Galapagos marine iguanas and explain how they arrived at and tested the hypothesis that sexual size dimorphism is sexually selected via direct male combat.
  4. What forms can male-male competition take besides combat? Give examples (including studies and evidence, as appropriate) of each. Describe the general "sneaky male" strategy and explain when it might be expected to be used.
  5. Describe the "direct benefits", "good genes", and "sensory bias" mechanisms for female choice. In what important way(s) do the direct benefit and good genes hypotheses differ from sensory bias? Discuss the studies that have evaluated these hypotheses and explain their findings. Are these mechanisms mutually exclusive?

Question from Dr. Dianne Byers, Illinois State University

  1. Why are females selective of their mates even in species in which males provide no material resources (e.g., food or parental care) to females or their offspring?

Chapter 11 -- Kin Selection

  1. What is Hamilton's rule?  How does it explain the evolution of altruism?
  2. What is the coefficient of relatedness and why is it important?
  3. Define and explain the significance of inclusive fitness. 
  4. What is direct fitness?  Indirect fitness?
  5. How can altruism spread when direct fitness is diminished?
  6. Why did J.B.S. Haldane mean when he said that he wouldn't sacrifice his life for one brother, but would to save two brothers or eight cousins
  7. Explain alarm calling in Beldings ground squirrel in terms of kin selection.
    1. Fully explain Figure 11.2
    2. Fully explain Figure 11.3
  8. Explain the evolution of nest helping in white-fronted bee-eaters
    1. Fully explain Figure 11.6
    2. Fully explain Figure 11.7
  9. Discuss kin selection in spadefoot toad tadpoles.  How is direct and indirect fitness affected by cannibalism?  How do cannibalistic tadpoles determine relatedness?  Why has this ability evolved?
  10. How are house mice able to determine which newborns to nurse in communal nests?  What is the advantage of this behavior?
  11. What are altruistic sperm?  Why did they evolve?
  12. [not discussed 2007] What is the evolutionary significance of being a "clever coot"?
  13. Why does haplodiploidy produce unusual coefficients of relationships (Fig. 11.12).
  14. What is haplodiploidy?  How has it been used to explain the evolution of eusociality?
  15. Does haplodiploidy explain the evolution of eusociality in insects?  Give three reasons.
  16. Fully explain what the phylogeny of the hymenoptera explains about the evolution of eusociality (Figure 11.13)
  17. Why is inbreeding considered to promote eusociality?  How does inbreeding affect the direct and indirect fitness of members of a eusocial colony.
  18. Why are ecological factors as, or more, important than inbreeding as a selective agent in promoting eusociality?
  19. Discuss kin recognition and how it is used in house mice to increase their inclusive fitness.
  20. Why is the strategy of remaining parents' nest and helping to raise siblings advantageous in bee-eaters and mole rats? What are the costs and benefits of founding a nest alone versus remaining with the parents?
  21. Why conditions have led to the evolution of eusociality in naked mole-rats?
  22. How does parent-offspring conflict affect direct and indirect fitness of parent and offspring?
  23. Discuss Figure 11.18a. 
    1. What does it indicate about optimum weaning time for the parent?  Why?
    2. What does it indicate about optimum weaning time for the offspring?  Why?
  24. Define reciprocal altruism.  Why has it evolved?  What are its costs?  What are its benefits?  Under what conditions will it be favored by natural selection?  How does it affect direct and indirect fitness?
  25. Discuss blood sharing in vampire bats as an example of reciprocal altruism.  Discuss and give examples of the aspects of their natural history that favor the evolution of this behavior.

Web Site Questions

  1. List and briefly describe the four possible outcomes of interactions among individual organisms. Which of these are not likely to be encountered in nature, and why?
  2. Explain why altruism is a central paradox of Darwinism. Discuss Hamilton�s concept of inclusive fitness, and discuss how this concept resolves the apparent paradox of altruism. Your answer should include Hamilton�s rule and a description of the terms of that equation. Compare and contrast direct and indirect fitness and clearly relate these to the process of kin selection.
  3. What evidence suggests that alarm calling in Belding�s ground squirrels has a fitness cost? Discuss Sherman�s evidence that this behavior has evolved via kin selection (frame your discussion in terms of specific predictions and tests). If self-sacrificing behavior is directed at close relatives and results in indirect fitness gains, is it truly altruistic? Explain why or why not.
  4. Under what conditions is helping at the nest usually found in birds? Why? Discuss Emlen and Wrege�s evidence that helping at the nest results in inclusive fitness gains for helpers. Can you think of other benefits these birds might gain from helping?
  5. Define eusociality and explain why this represents the "epitome of altruism." Explain the haplodiploidy hypothesis for eusociality in hymenopteran insects and discuss the evidence for and against this hypothesis. Be sure your discussion includes specific predictions and tests. How does sociality in paper wasps differ from that in eusocial hymenopterans? Discuss the costs and benefits of each of the strategies employed by this group.
  6. Describe the social system in naked mole rats, and discuss the evidence that a combination of inbreeding and ecological factors explain the evolution of eusociality in this species.
  7. Why is parent-offspring conflict expected to be particularly sharp in birds and mammals? Explain the principle of weaning conflict by discussing the costs and benefits of weaning from the perspective of a mother, one of several full siblings, and one of a litter of half-siblings. Discuss the evidence that harassment in white-fronted bee eaters are attempts by fathers to break up the nesting attempts of their sons in order to recruit those sons to help at their own nests.
  8. What is siblicide? Discuss Lougheed and Anderson�s evidence that masked booby parents are more tolerant of siblicidal offspring than are blue-footed booby parents. What hypotheses might explain this difference? How would you test them?
  9. Define reciprocal altruism. What kind of cooperation can this process explain, and what conditions are necessary for it to operate? Given those conditions, in what kinds of organisms might we expect to find it? Discuss Wilkinson�s evidence that reciprocal altruism explains altruistic feeding behavior in vampire bats. Is reciprocal altruism really altruistic, as altruism is defined in this chapter? Why or why not?

Questions from University of Missouri, Rolla, Dr. Ronald Frank

  1. What are the four types of social interactions? Indicate the cost or benefit to the actor and the recipient in each case. Which type is not found abundantly in nature? 
  2. What does the following formula predict: Br - C > 0
  3. What simple formula is used to predict whether an altruistic behavior will increase in frequency in a population? 
  4. Describe inclusive fitness and clearly define its two components. What evidence indicates that kin selection is at work in populations of Belding's Ground Squirrels? 
  5. Why do females of Belding's Ground Squirrels sound alarms more often than males?
  6. What evidence indicates that kin selection is at work in populations of White-Fronted Bee Eaters? 
  7. Kin selection implies kin recognition. What are the two types and what evidence suggests that each one exists in natural populations? 
  8. Why do some yearling White-Fronted Bee Eaters return to their parents nest after attempting to mate on their own? Indicate why the mechanism is successful. 
  9. Under what conditions would siblicide be beneficial to parents? 
  10. What is eusociality? Name the three characteristics of eusociality.
  11. Describe the kin selection component of eusociality in Hymenoptera. What other environmental factors may contribute to eusociality? 
  12. What is reciprocal altruism? What are the two conditions that describe the interaction? What are the three conditions that describe the social environment in which it's found? 

Chapter 13 -- Evolution and Human Health

  1. What is meant by host/pathogen coevolution?  Explain the role of natural selection in this process.
  2. Why is host-pathogen coevolution referred to as an �evolutionary arms race�?
  3. In what sense(s) are pathogens and hosts in conflict?
  4. How is the Influenza A virus similar to the HIV virus?  How does it differ?
  5. What are the two most important mechanisms for evolution in the flu virus?
  6. What is the evidence that natural selection is more important than drift in hemagglutinin evolution in the flu virus?
  7. What is positive selection?  What is the evidence for positive selection in the Influenza A virus.
  8. What is the evidence for gene swapping in 1968 flu pandemic?
  9. Why is the Influenza A virus such a potentially lethal pathogen?
  10. What likely caused the global flu pandemic of 1968?
  11. Discuss the evolution of antibiotic resistance?  Explain the role of natural selection in this process.  Does this have any costs to bacteria?  What should we be doing to limit antibiotic resistance?.
  12. What causes antibiotic resistance in pathogens?
  13. Why are there costs to evolve antibiotic resistance?
  14. Why has reduced antibiotic use led to decreased pathogen resistance in some pathogens?
  15. Discuss the three hypotheses have been proposed to explain the evolution of virulence.  Explain the role of natural selection in these processes.
  16. What is the coincidental evolution hypothesis to explain the evolution of virulence?  Give an example.
  17.  What is the short-sighted evolution hypothesis to explain the evolution of virulence?  Give an example.
  18.  What is the trade-off hypothesis to explain the evolution of virulence?  Give an example.
  19. Use the transmission rate hypothesis to explain the virulence of HIV-1.
  20. Discuss the experiment of Messenger et al. (Fig. 13.9) that demonstrated the relationship of phage virulence to length of vertical transmission period.
  21. Why are vectorborne pathogens more virulent than those that are transmitted directly?
  22. Discuss the evolution of virulence in vectorborne versus directly transmitted diseases. (Fig. 13.10)  Explain the role of natural selection in this process.
  23. Discuss the evolution of virulence in intestinal bacteria as a function of the tendency toward waterborne transmission (Fig. 13.11).  Explain the role of natural selection in this process.
  24. Myopia is heritable.  Why are the allele(s) for it maintained in a hunter-gatherer society such as the Inuit where it is a disadvantage?
  25. Discuss the evidence that myopia is maladaptive only in our present environment.  Explain the role of natural selection in this process.
  26. [not discussed 2007]Is fever adaptive in ectotherms?  What is the evidence?
  27. [not discussed 2007]Is fever adaptive in humans?  What is the evidence?
  28. What is the evidence  that continuous menstrual cycling is maladaptive?  What is the likely cause of  a much higher incidence of breast cancer in women who follow western urban lifestyles than women, such as the Dogon who follow traditional lifestyles, do not?
  29. [not discussed 2007] Discuss how evolution may be able to explain some maladaptive human parenting behavior.

Web Site Questions

  1. In what sense(s) are pathogens and hosts in conflict?
  2. Outline the structure of the influenza A virus and briefly relate that structure to human immune response to the virus.
  3. Discuss the reasoning behind, and evidence for, the hypothesis that flu pandemics begin when human and bird strains of influenza A simultaneously infect a pig, swap genes, then infect people.
  4. Describe the reasoning behind Fitch et al.'s hypothesis that flu strains with novel antigenic sites should enjoy a selective advantage. Discuss the specific predictions and tests of their hypothesis, and explain how their findings may be useful for predicting which circulating flu strains are most likely to have surviving descendants (be sure to include any relevant evidence that this approach actually works). Is this the same as predicting which strain(s) will be responsible for a subsequent year's epidemic? Explain
  5. Define virulence. Compare and contrast the "coincidental evolution", "short-sighted evolution", and "trade-off" hypotheses for the evolution of virulence.
  6. Discuss Ewald's application of the trade-off hypothesis for the evolution of virulence to human pathogens by explaining the reasoning behind his specific predictions about how differences in transmission mode should result in differences in virulence. How did he test these predictions, and what did he find? What are the general and specific implications of these findings for the effect of human behavior on the severity of human diseases?
  7. [not discussed 2007] Illustrate the fact that tissues within organisms can follow their own "evolutionary trajectories" using Hirschhorn et al.�s studies of the ADA patient who spontaneously recovered from this serious genetic disease. If Hirschhorn et al. are correct in their hypothesis for the mechanism of recovery, what are the implications for the current practice of using enzyme replacement therapy in conjunction with somatic gene replacement therapy for this disease?
  8. Using the information provided, evaluate the hypothesis that alleles predisposing people to myopia have not been selected against historically because those alleles do not cause myopia in hunter-gatherer environments. What additional studies would strengthen that conclusion?
  9. Discuss the evidence that continuous menstrual cycling is a maladaptive consequence of modern urban lifestyles. How strongly does the fact that the breast cancer rate in urban West African women is about one-twelfth that of North American women support this hypothesis? Explain.
  10. [not discussed 2007] Describe the pattern of parenting behavior found in male reed buntings and discuss the evidence supporting the hypothesis that males are selectively directing parental care toward their own offspring. In what sense can we legitimately say that the male's genotype determines parental effort, and in what sense can we not say so?
  11. [not discussed 2007] Discuss Flinn's observational study of parent-child interactions in rural Trinidad, clearly identifying the hypothesis he was testing, the methods he used to do so (including relevant controls), and his findings. How do these compare to the findings in the study of reed buntings? What evidence do studies of other cultures provide that this pattern may be widespread in humans? Discuss Flinn and England's and Daly and Wilson's evidence that discrimination by parents against stepchildren has public-health consequences. Do these studies suggest that antagonism toward stepchildren is adaptive? Explain
  12.  


    Chapter 15 -- Mechanisms of Speciation

    1. Define, give examples of, and explain the evolutionary significance with regard to speciation of
      1. anagenesis
      2. cladogenesis
      3. lateral gene transfer
      4. biological species concept
      5. morphological species concept
      6. phylogenetic or evolutionary species concept
      7. sibling or cryptic species
      8. allopatric speciation
      9. dispersal
      10. vicariance
      11. polyploidy
      12. chromosomal fissions and fusions
      13. genetic drift
      14. natural selection
      15. sexual selection
      16. sympatric speciation
      17. secondary contact
      18. hybridization
      19. reinforcement
      20. prezygotic isolating mechanisms
      21. postzygotic isolating mechanisms
    2. What are the advantages of the biological species concept?  The disadvantages?  What does it have in common with other widely usd species definitions?
    3. Regarding the red wolf 
      1. What is the evidence that the red wolf deserves protection under the terms of the endangered species act. 
      2. What are the implications if this is correct.
      3. What is the evidence that the red wolf does not deserve protection under the terms of the endangered species act. 
      4. What are the implications if this is correct. 
    4. Explain and compare and contrast isolation by dispersal and isolation by vicariance.
    5. What is the difference between allopatric and sympatric speciation?   How are allopatric and sympatric speciation similar?
    6. Is isolation essential for speciation?  Discuss its role in allopatric and sympatric speciation.  How do vicariance and dispersal differ as mechanisms promoting isolation?
    7. How does Figure 15.7 suggest that speciation in Hawaiian Drosophila is the result of dispersal events?  Include a discussion of the geologic history of these islands as it relates to speciation.
    8. Discuss the stages and mechanisms involved in the evolution of Caribbean and Pacific snapping shrimp. What is the evidence that supports this hypothesis.
    9. What are the three most important mechanisms for genetic divergence in the speciation process?  Which is the most important?  Why?  The least important?  Why?
    10. Regarding Rhagoletis, the maggot fly.
      1. Are the flies that parasitize apples and hawthorns distinct races? Why is this an unexpected conclusion? 
      2. What has led to the divergence of the apple and hawthorn races? Be specific about the processes involved.  Explain the role of natural selection in these processes.
      3. What are the three factors that led to the switch to apples? (i.e., the three factors that increase fitness by laying eggs on apples rather than on hawthorn fruit) 
      4. What conclusions about evolutionary processes can be drawn from this?
    11. Divergent populations come can back into secondary contact 
      1. What are the two major possible outcomes of this process? 
      2. What are the three possible outcomes of hybridization?
      3. What favors and promotes reinforcement? 
      4. How can genetic engineering cause potential problems? 
      5. What is the significance of hybridization to plant evolution? 
      6. What factors promote genetic isolation even if there is no immediate contact between isolated populations?
    12. Define the two major classes of reproductive barriers between closely related species?  Discuss the major examples of each of the two.
    13. Discuss the reinforcement processes at work promoting the genetic divergence of maggot flies.

    Web Site Questions 

    1. Outline the three general stages of speciation. Describe Mayr�s general allopatric model of speciation. Which of the three general stages does this model describe? Compare and contrast the dispersal and vicariance as isolating mechanisms, and discuss how these two hypotheses can be tested using Hawaiian fruit flies and Central American snapping shrimp as your example. For each example, be sure to clearly identify the predictions each hypothesis would make, then discuss the available data in light of those predictions. 
    2. Discuss the mechanism(s) by which a change in chromosome number may act as a barrier to gene flow. In what organisms is this mechanism thought to have been important, and what evidence supports this view? Is a difference in chromosome complement necessarily evidence that the change in chromosomes caused genetic isolation? Why or why not?
    3. Discuss the potential role of genetic drift as a mechanism of genetic divergence among isolated populations. Under what conditions is drift thought to be most likely to lead to divergence? Are these conditions likely met in nature? Defend your answer. Is drift currently considered to make a major contribution to divergence and speciation? Why or why not?
    4. Describe the role of natural selection as a mechanism of genetic divergence using apple and hawthorn maggot flies to illustrate your answer. What mechanism is thought to have isolated these populations? What evidence suggests that genetic divergence has occurred and that natural selection is the mechanism responsible? Is divergence due to host and/or habitat switching rare or common? Defend your answer.
    5. Can sexual selection contribute to the genetic divergence of isolated populations? If so, is it likely to be any more or any less "efficient" than natural selection? Why or why not? Illustrate your answer using Hawaiian fruit flies, being sure to identify the key predictions and tests of the sexual selection hypothesis.
    6. Explain Dobzhansky�s hypothesis of reinforcement and its role in completing reproductive isolation between genetically divergent populations. If reinforcement acts, what kind(s) of isolating mechanisms should result? What kind(s) of isolating mechanisms might arise in the absence of reinforcement? Discuss evidence from lab, field, and modeling studies about the role and prevalence of reinforcement in completing reproductive isolation.
    7. Do hybrid offspring between genetically divergent parents always have reduced fitness? Relate your answer to the concern some biologists have expressed about the potential "escape" of genetically engineered plant alleles into weedy relatives of crop plants. Use Arriola and Ellstrand�s work on sorghum to illustrate your answer. Then discuss Rieseberg et al.�s work on hybrid sunflowers, and describe their evidence that hybridization may result in the formation of new species.
    8. Explain the reasoning behind the traditional view that a radical reorganization of the genome was necessary to produce new species. Is this view currently held? Why or why not? Describe Haldane�s rule (including the evidence that it is pervasive) and discuss Muller�s hypothesis to explain it. What genetic evidence supports this hypothesis?

    Questions from Dr. Kilburn's webpage

    1. Defend the view that species are real entities. Compare and contrast the morphological (typological and phenetic) and biological species concepts. What are the strengths and weaknesses of each? For what group(s) of organisms does each work well and for what groups does each work poorly. Why? Be sure to define all relevant terms. Is the red wolf a valid biological species? Why does the answer matter? Defend your answer.
    2. Compare and contrast anagenesis (phyletic change) with cladogenesis. Which represents "true" speciation (i.e., produces an increase in the number of species)
    3. Outline the three basic steps of cladogenesis. Compare and contrast allopatric speciation with sympatric speciation in terms of the geographic distribution of diverging species proposed by each. What kinds of barriers to gene flow do allopatric speciation models propose? Define and give examples of both dispersal and vicariant events and explain how each can be tested using the examples in the text to illustrate. What kinds of barriers to gene flow do sympatric speciation models propose? Outline the basic process by which each can produce a barrier to gene flow, using relevant examples to illustrate your answer.
    4. Explain the role played by genetic drift and natural selection in causing the genetic divergence of isolated populations. Discuss Mayr's model of allopatric speciation by peripheral isolation. Does the current evidence support as important a role for genetic drift as he proposed? Explain. Using the example of Rhagoletis pomella to illustrate, describe how selection can promote genetic divergence of isolated populations. Be sure to include the experimental tests of the relevant hypotheses in your answer.
    5. Describe Dobzhansky's reinforcement hypothesis for the evolution of reproductive isolating mechanisms. What is the current evidence for the importance (or non-importance) of reinforcement? Outline the major reproductive isolating mechanisms as classified by Dobzhansky, being sure to define and give an example of each.
    6. Discuss the range of outcomes that can occur when reproductive isolation is incomplete. Relate these outcomes to the concern some scientists have expressed over the potential for the evolution of "superweeds". Are their concerns justified? Explain using Arriola and Ellstrand's experiments on sorghum and johnsongrass to support your answer.