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

REVIEW QUESTIONS - Introduction

  1. What did Dobzhansky mean by the statement "Nothing in Biology Makes Sense Except in the Light of Evolution."
  2. What is evolution a fact?
  3. Why is evolution a theory?

REVIEW QUESTIONS - CHAPTER 1

  1. Using the information in Figure 1.1, discuss how the HIV/AIDS pandemic differ s in sub-Saharan Africa versus North America.
  2. What is a retrovirus?  How are retroviruses similar to other kinds of viruses?  How do retroviruses differ from other kinds of viruses?
  3. See Figure 1.3.  What accounts for successful HIV/AIDS prevention?
  4. See Figure 1.4.  What is this figure showing about rates of new HIV diagnoses?  Why?
  5. How do retroviruses reproduce ? Include all the steps in the life history of the HIV virus. [see Fig. 1.5, The life cycle of HIV]
  6. How do viruses recognize which cells they have evolved to infect?  How do they attach to the host cell?
  7. What are the molecular and evolutionary significances of replication using reverse transcriptase rather than DNA polymerase? Explain why there are these differing results.
  8. Discuss the roles of CD4, reverse transcriptase, and integrase in the infection of a T cell by HIV? [see Fig. 1.5, The life cycle of HIV]
  9. How does HIV cause AIDS?
  10. See Figure 1. 8, progression of untreated HIV infection .  Discuss what is happening to the CD4-T-cell count during the acute, chronic, and AIDS stages of an HIV infection.  Explain why.
  11. See Figure 1. 8, progression of untreated HIV infection .  Discuss what is happening to the viral load during the acute, chronic, and AIDS stages of an HIV infection.  Explain why.
  12. What is the difference between AZT and thymidine that enable it to function as an anti-HIV drug.
  13. How does AZT function as an antiAIDS drug?
  14. Why does AZT usually not interfere with normal cellular transcription (i.e. DNA to mRNA)? 
  15. Why could AZT potentially cause problems with replication?  Why is it unlikely that AZT could cause problems with transcription?
  16. Why do retroviruses such as HIV evolve resistance to drugs such as AZT so rapidly?
  17. What is the evidence in Fig. 1.11, that HIV populations evolve resistance to AZT.
  18. Why does AZT fail in the long run? What mutations are responsible for this failure. In what molecule and where are these mutations expressed?
  19. Does AZT cause the mutations which result in HIV strains resistant to AZT?  If yes, explain how.  If no, explain how HIV becomes resistant.
  20. What is the "cost" to a population of HIV viruses that has evolved HIV resistance?  Why?
  21. What is the nature of the mutation that causes AZT sensitivity in HIV? (see figure 1.13)  What is the advantage of this mutation?  The disadvantage?
  22. 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.
  23. Is evolution by natural selection unidirectional and irreversible? Why or why not?  Use evidence from the use/disuse of AZT to justify your answer.
  24. What is the advantage in having a high mutation rate in the gene that codes for reverse transcriptase?
  25. 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.
  26. Explain figure 1. 14, How HIV populations evolve resistance .  Discuss the evidence four the evolutionary steps (see section 3.2, Darwin's four postulates ) involved .
  27. What is the evolutionary rationale behind Highly Active Anti-Retroviral Therapy (HAART)?
  28. 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?
  29. Why is HIV Fatal? Explain in terms of the proximate cause (how).
  30. Why is HIV Fatal? Explain in terms of the ultimate cause (why).
  31. 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.
  32. Why do retroviruses have much higher mutation rates than most nuclear genes?
  33. What is the advantage of having a high mutation rate in the gene that codes for reverse transcriptase?  What are the costs?
  34. In Figure 1.17a, evolution of the HIV population.  What is the significance of an increasing genetic distance?  What is occurring during years 0-6?  Explain why there is a decrease in mutation accumulation after year 6.
  35. Evolution in HIV can be described as short-sighted.  Explain why.
  36. 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.
  37. What is virulence?  What enables a pathogen to be highly lethal?
  38. What is the correlation between lethality and transmission of HIV?  What does this indicate about the best strategies in the fight against AIDS?
  39. How does HIV enter cells?
  40. What is the molecular basis (CCR5-delta32) that causes some people to be resistant to infection by HIV?
  41. Explain Fig.1.20, frequency of the ccr5-delta 32 allele.  What caused this geographic distribution?
  42. 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.
  43. What does HIV phylogeny show about how the virus has moved between host species. What does it indicate about the origin of AIDS?
  44. On figure 1.2 1 , 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.
  45. From figure 1. 21 , what is the evidence that transmission of HIV from an SIV relative in non-human primates to humans has taken place multiple times?
  46. In Figure 1.2 1 a,  HIV-1 is closer to SIVcpz and HIV-2 is closer to SIVstm. What does this imply about the evolutionary history of HIV? 
  47. In Figure 1.2 1 a, 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? 
  48. 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?  
  49. What is an epitope?  What is the advantage of having a high mutation rate in the genes that code for them?
  50. What is a vaccine? Explain the molecular basis of how they work.  Include a discussion of epitopes.
  51. 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.
  52. Why is HIV/AIDS denialism similar to evolution denialism?

REVIEW QUESTIONS--CHAPTER 2  For all of your answers EXPLAIN fully with examples as needed. 
  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 or molecular homology 
    4. Analogy 
    5. Parsimony 
    6. Vestigial structure 
    7. Developmental vestigial trait
    8. Pseudogene 
    9. Processed pseudogene
    10. Direct observation of change through time 
    11. Fossil record 
    12. Transitional forms 
    13. Ring species
    14. Extinction 
    15. Law of succession 
    16. Geologic time scale 
    17. Radiometric dating
  2. What is microevolution ?  What is macroevolution?  Are the two necessarily different from each other?   How are they similar?
  3. What is the "Theory of Special Creation" (Fig. 2.1)?  Is it supported by the fossil record and molecular genetics?  Give the evidence for or against.
  4. Box 2.1 discusses the Fact of Evolution and the Mechanism of Evolution.  What is meant by each term?
  5. Explain what figure 2.3a (evolutionary change in soapberry bugs) shows.
  6. Explain what figure 2.3b (evolutionary change in soapberry bugs) shows.
  7. What was the evolutionary response of soapberry bugs to the introduction of flat-podded golden rain trees in Florida?
  8. Referring to Figure 2.3 , 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 7 6 .  Discuss what, if anything, on the figure supports each of the postulates.
  9. What is the function of arrector pilli muscles (Fig. 2.5)?  Why do humans have them?
  10. Why is the pattern of the development of digits in chickens (Fig. 2.6) better explained by evolution rather than special creation?
  11. How did Cuvier demonstrate the fact of extinction?  Why was this important in challenging the dominant European worldview of the time?
  12. How has the fossil record of the origin of birds provided evidence for evolution?
  13. How has the fossil record of the origin of whales provided evidence for evolution?
  14. What is biological plenitude and how did Cuvier demonstrate it was false?
  15. What is the Scala Naturae and why does it present an incorrect picture of the history of life?
  16. What are phylogenetic trees?  Why did Darwin consider them so important?
  17. Explain how evolutionary trees describe histories of descent with modification (e.g., Fig. 2.14g)
  18. How does the Siberian greenish warbler provide evidence that one species can split into two (Fig. 2.17)?
  19. Explain why the bones in the forelimb of bats and birds are homologous, but bat wings and bird wings are analogous. 
  20. Give an example of a nonhomologous similarity.  Does this pose a problem for evolutionary biology?
  21. How do developmental homologies in the vertebrates (Fig. 2.20) provide evidence for evolution?
  22. Why doe the genetic code (Fig. 2.22) provide evidence for evolution?
  23. How and why does unequal crossing over produce genetic flaws?
  24. Why do the shared genetic flaws such as that illustrated in figure 2.23 better explained by evolution than by special creation.
  25. Draw a cladogram showing the distribution of the six processed pseudogenes for the seven taxa of Fig 2.24c.  Why does this provide evidence for common ancestry?
  26. How did Charles Lyell influence Darwin's ideas?
  27. What is the difference between relative dating and absolute dating?  Why does the use of both of them together provide strong evidence for evolution?
  28. What is methodological naturalism?  How does it differ from ontological naturalism?
  29. Why is it necessary for a scientist to apply at least methodological naturalism, if not ontological naturalism, to the study of biological processes?
  30. Questions from the 4th edition website (http://wps.prenhall.com/esm_freeman_evol_4/75/19386/4963061.cw/index.html)
    1. Look again at textbook Figure 2.3b, which shows beak lengths of soapberry bugs over time. What happened to variation in beak length when the golden rain trees appeared? Did soapberry bugs with new beak lengths (not seen before in the population) appear after the introduction of golden rain trees? Comment on what this pattern shows about the initial stages of evolution.
    2. What surprising thing do bird embryos' feet and wings do during development? What is the significance for evolutionary theory?
  31. FROM THE 3rd EDITION REVIEW QUESTIONS   (These also apply to the 4th edition!!)
    1. Briefly explain why shared "flaws", such as the presence of the proximal CMT1A repeat (SEE FIGURE 2.23 ), 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?
  32. FROM THE 2nd EDITION REVIEW QUESTIONS (These also apply to the third and 4th 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 For all of your answers EXPLAIN fully with examples as needed. 
  1. Define the following terms. Explain, using examples, how each is involved in evolution.
    1. Darwinian fitness
    2. adaptation
    3. heritability
    4. reproductive potential
    5. exaption
  2. Why did Darwin devote a chapter in the Origin of Species to artificial selection?
  3. Why does understanding the role of the fw2.2 gene in genetically manipulated tomatoes increase our understanding of natural selection?
  4. Explain how the interaction between the pack rat and the chilies (Fig. 3.4) produces decent with modification.
  5. Which of Darwin's four postulates do the snapdragons shown in Figures 3.5a, b, and c demonstrate.  Explain.
  6. Why does figure 3.6, diversity of Darwin's finches, demonstrate evolution?
  7. Why is beak shape an important attribute for an evolutionary biologist to study?
  8. Why are the Galapagos Islands such an excellent laboratory for evolution?
  9. Be sure to explain the figure completely. Thinking about how the Finch bill demonstrates Darwin's Four postulates,
    1. What does figure 3. 9 demonstrate?
    2. What does figure 3. 10 demonstrate?
    3. What does Figure 3. 12 demonstrate?
    4. What does Figure 3. 13 demonstrate?
    5. What does Figure 3.1 4 demonstrate?
  10. Why is the regression line 1978 above that of 1976 in Figure 3.10?
  11. Why does the study of bone morphogenetic protein 4 and beak development (Fig. 3.11) increase our understanding of speciation by the Galapagos finches?
  12. Do Figure s 3. 12a and b 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 explanation could account for the correspondence between the two?  Assuming the answer is yes, why isn't the correlation perfect?
  13. What is the role of reproductive potential in Figure 3.12a and 3.13?
  14. What do Figures 3.15 a, b, c (30 years of evolution) demonstrate about the evolution of ground finches?
  15. What are the roles of individuals and populations in natural selection?
  16. What are the roles of phenotypes and genotypes in evolution?  If the phenotype is not controlled by the phenotype, what will selection cause?
  17. Explain why a genetic basis for a trait is necessary the trait to evolve in response to natural selection.
  18. 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'."
  19. Why can't evolution purposely produce adaptations that will be needed for future conditions?
  20. Discuss how evolution via "natural selection can produce new traits, even though it acts on existing traits." (e.g., Fig. 3.18, oil in corn)
  21. Can a trait arise "for the good of the species"? Explain using examples of how altruistic behavior evolves.
  22. Define and give examples of �preadaptation' and �exaption.' What do they indicate about the nature of the evolutionary process.
  23. Discuss the "panda's thumb" , gonopodia in Gambusia, 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?
  24. What would be the perfect beak shape in Geospiza fortis during droughts?  Why don't we see this shape?  Is this evidence for evolution or special creation?
  25. What were the three most serious problems with Darwin's original proposals.
  26. Why did blending inheritance pose a problem for Darwin?
  27. Why did Lord Kelvin pose problems for Darwin's conception of evolution occurring gradually in small steps?
  28. Are evolutionary biologists using a tautology when they refer to �survivial of the fittest?'
  29. Creationists claim that the vertebrate eye is much to complex and involves so many dependent features to have evolved.  Why is this false?
  30. Why is using "Irreducible Complexity" to support special creation criticized as "an argument from credulity?"
  31. Explain how the example of gene co-option in Figure 3.25 supports evolution rather than special creation.
  32. Why is exaption important for evolution?
  33. 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. 9 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. 10 , 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.
  34. 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?
  35. FROM THE 2nd EDITION REVIEW QUESTIONS (These also apply to the third and 4th edition s !!)
    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 5 For all of your answers EXPLAIN fully with examples as needed. 
  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 5.5a, How do mutations affect fitness.
  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 5.10) 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 5.3.
  23. Explain and discuss Figure 5.12, electrophoresis to determine CCR5 genotypes.
  24. Explain and discuss Figure 5.13, "Analysis of proteins."
  25. Explain and discuss Figure 5.14 "Sequencing the CF locus in humans."
  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 6 For all of your answers EXPLAIN fully with examples as needed. 
  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. [not covered 2009] 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. [not covered 2009] 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. Scale- eating fish a dominant "right-handed" allele frequency of  about 0.3.  Use Hardy-Weinberg to explain why this this is necessary if the left handed and right  phenotypes are both 50% .

Review questions -- CHAPTER 6

  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 6 .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. Explain the experiment summarized in Figure 6.13 showing the frequencies of an allele in four populations of fruit flies over 50 generations.
  6. Apply the reasoning developed in your answer to the previous question to the three HIV/CCR5delta32 scenarios in Figure 6 .15.  What are the implications for evolution changing HIV resistance in Europe and Africa?  Why?
  7. 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?
  8. 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)?
  9. Explain the change in frequency of the dominant and the lethal recessive alleles over time as illustrated in Fig. 6 .16 for flour beetles
  10. 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.
  11. 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
  12. For figure 6.18, explain why the non-lethal allele if it is initially has a very high frequency (e.g., close to 100%) decreases until it reaches the equilibrium value?

  13. What is frequency-dependent selection?  How does it maintain the two color morphs of the Elderflower orchid?

  14. Why is mutation by itself such a weak mechanism of evolution?

  15. What does figure 6.25 showing cell size in E.colli indicate about the interaction between mutation and selection?  Explain.

  16. [not covered 2009] What is mutation selection balance?  Why can the frequency of Spinal muscular atrophy be explained by mutation selection balance?

  17. [not covered 2009] Why can't the frequency of cystic fibrosis be explained by mutation selection balance? How can it be explained?

    [FROM THE SECOND EDITION]

  18. Fully explain why most sexually reproducing species have 50% males and 50% females.
  19. Discuss the significance of Fig. 6 .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 6 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 6 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. [not covered 2009] 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]
  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. [not covered 2009] 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. 6 .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. Calculate the frequency of each genotype and of each allele. Is the population in Hardy-Weinberg equilibrium? Why or why not?

Chapter 7 - Review questions For all of your answers EXPLAIN fully with examples as needed. 
  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. Figure 7 .7 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. Define and give examples of the founder effect. Discuss its effect on Hardy - Weinberg equilibrium, genetic diversity, allele frequency, and evolution.
  8. What is inbreeding and what is its effect on allele and genotype frequencies?
  9. Explain Figure 7.13c.  What is happening to allelelic diversity in the silvereye?  Why?
  10. Using Figure 7 .15 a, b, and c , explain how population size affects genetic drift.
  11. Using Figure 7 .15 d, e, and f , explain how population size affects genetic drift.
  12. How does drift cause alleles to become fixed or lost?
  13. Discuss the significance of allele frequency changes over 19 generations in Figure 7 .16.
  14. In Figure 7.17 showing Buri's experiment, why is fruit fly heterozygosity declining over 20 generations?
  15. In Figure 7.17 showing Buri's experiment, why is fruit fly heterozygosity for the 16 flies in the experiment tracking the curve for a population of 9 flies rather than the upper curve for 16 flies?
  16. Discuss the factors responsible for the pattern of genetic variation seen in populations of collared lizards in the Ozarks (Fig. 7 .18)
  17. Discuss the interactions of genetic drift and selection on mutations of different fitness from a neutral and a selectionist point of view.
  18. According to the neutral model, what is the only role for natural selection in evolution?
  19. According to the selectionist model, what is the most important role of selection in evolution?
  20. Are neutral mutations most affected by drift or selection? Why?
  21. 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 .
  22. What observations on the molecular evolution of the influenza virus provides evidence for the neutral theory of evolution?
  23. Explain figure 7.21c.  Why do synonymous mutations occur at a higher rate than non-synonymous mutations?  What does this indicate about evolutionary processes?
  24. What is the evidence for positive selection shown in Figure 7.23, the cladogram with mutation rate ratios for the BRCA1 gene?
  25. How does inbreeding affect the genetic structure of a population?
  26. 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?
  27. 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.
  28. Why does the genotype distribution for the PAP allele of 33 sea otters (SS =16, SF = 7, FF = 10) indicate they are inbred?  Show your calculations that demonstrate this.
  29. What is the evidence for inbreeding depression in humans? Draw a graph that illustrates this effect.
  30. How can genetic drift, gene flow and inbreeding affect threatened species? Discuss how efforts to conserve biodiversity can address each of these processes .
  31. In what ways does habitat fragmentation specifically pose a threat to species survival?
  32. How have habitat destruction, deleterious alleles, genetic drift, inbreeding depression, migration, and nonrandom breeding affected the population genetics of the greater prairie chicken?
  33. Why was the genetics of museum specimens of prairie chickens studied in trying to understand what happened to the Illinois population?  What was learned?
  34. Why was the Illinois Greater Prairie Chicken experiencing a "mutational meltdown"?
  35. Why did the introduction of outside migrants potentially rescue the Illinois Greater Prairie Chicken?

Chapter 7 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 7 - 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. Explain the founder effect using relevant examples.
  5. 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 
  6. 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 and Templeton et al.'s studies of Ozark collared lizards. 
  7. 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. 
  8. 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?
  9. 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?
  10. What is inbreeding and what is its effect on allele and genotype frequencies? Does inbreeding cause evolutionary change? Why or why not? 
  11. 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. 
  12. 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. 
  13. Define the term "inbreeding depression" and illustrate using human infant mortality and reduction in hatching success in great tits.  
  14. 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 8 For all of your answers EXPLAIN fully with examples as needed. 

  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. What does it mean if a population is in linkage equilibrium?
  7. 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. 8.2a)?
    2. What is the expected frequency of the 16 genotypes (Fig. 8.3a)?
  8. How does sexual reproduction reduce linkage disequilibrium?
  9. Fully explain Figure 8.6.
    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?
  10. Fully explain Figure 8.7.  Why is linkage disequilibrium changing?  What does a a value of 1 or -1 indicate?  a value of 0?
  11. 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.
  12. What are the advantages of asexual reproduction.  Explain the significance of Figure 8 .17 in terms of this.
  13. Why does asexual reproduction give a reproductive advantage?  Give a numerical example to illustrate the reproductive advantage.
  14. What are the disadvantages of sexual reproduction?
  15. In Dunbrack et al.�s experiment with Tribolium (Fig. 8.18), explain
    1. how were the asexually evolving populations simulated?  Is this a reasonable way to do this?
    2. when the simulated a sexual 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 .
  16. What are the advantages of asexual reproduction.  Explain the significance of Figure 8 .18b and d in terms of this.
  17. What are the advantages of sexual reproduction. Explain the significance of Figure 8 .18a and c in terms of this.
  18. Figure 8 .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?
  19. Explain how Muller's ratchet affects sexual populations differently from asexual populations
  20. Explain how Mueller's ratchet (Fig. 8 .20) can explain the results of Andersson and Hughes' experiment (figure 8 .21).
  21. How do periodic bottlenecks in bacteria (Fig. 8 .2 1 ) demonstrate Muller's ratchet?  What caused some of the bacterial populations to develop decreased fitness?
  22. Why are the shortcomings of Mueller�s ratchet as an explanation for the evolution of sexual reproduction.
  23. What is the Red Queen hypothesis?
  24. How does the Red Queen hypothesis explain the evolution of sexual reproduction?
  25. What is the evidence that sex is an adaptation to short-term change?
  26. Discuss figure 8 .22 .   How  does a host parasite arms race make sex beneficial ?
  27. How does the study on New Zealand snails (Fig. 8 .23) support the host parasite arms race hypothesis for the evolution and maintenance of sexual reproduction?
  28. Explain how the Red Queen hypothesis explains why sex is advantageous in the face of parasites or disease .
  29. In Lively�s study of New Zealand snail populations (Fig. 8.23), why are males less common in populations with low parasite infection rates?
  30. In Lively�s study of New Zealand snail populations (Fig. 8.23), 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. 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.
  4. Describe the experimental and theoretical work addressing the assumptions of Maynard Smith's model. What general conclusion can be drawn about those assumptions?
  5. 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?
  6. 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.
  7. 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 9 For all of your answers EXPLAIN fully with examples as needed. 

  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. 9.2)?
  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 9.13a, b, ,c, and d.  What can you conclude about the relationship of offspring height to parent height from each one?  Why?
  8. What does figure 9.13d 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 9.14. 
    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. What does the top graph indicate about environment?   Why?
    6. What does the bottom graph indicate about environment?   Why?
    7. 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)?
  13. What can hereditability be used to determine?  What cant it be used to determine?
  14. Alpine Skypilots:
    1. Discuss the significance of the following three figures ( 9.20 , 9.21 , 9.22 ) 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 9.20?  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 response to selection (R) determined by Galen is 5%?
  15. What are the three modes of selection?  How does each affect the average value and variation of the character being studied?
  16. How does directional selection differ from stabilizing selection?  from disruptive selection? How does disruptive differ from stabilizing?
  17. Give examples of the three modes of selection.
  18. Why is it expected that most of the time stabilizing selection should be the most common?
  19. Why is there stabilizing selection on human birth weight?
  20. Discuss and explain the selection factors at work and their results on the gall-making fly (Figure 9.26 ).
  21. Discuss and explain the selection factors at work and their results on the black-bellied seed cracker (Figure 9.27 )
  22. What causes a trait to have high heritability?  In Fig. 9.28, both populations have the same heritability for height.  Why? What does this experiment tell us about attributing genetic causes to differences between populations?
  23. What does heritibility tell us about genetic differences between populations?  Why?
  24. What does heritibility tell us about differences within populations?  Why?
  25. [Omit] Figure 9.29 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.   
  26. [Omit] 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?
  27. [Omit] 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?
  28. 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. 9.31 )
  29. Yarrow plants alt low altitudes make more stems than yarrow plants at high altitudes.  Studies have shown that number of stems has a strong genetic component (assume h2 is close to 1).  What does this indicate about the role of genes being responsible for the differences between the two populations?
  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. 9.31).  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 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?
  5. [Omit] 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?
  6. 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.
  7. 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 10 Adaptation For all of your answers EXPLAIN fully with examples as needed. 

  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. [Omit] 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. Explain what figures 10.2, 10.3, and 10.4 show about the co-evolutionary relationship between oxpeckers and cattle.
  5. Why must evolutionary hypotheses be tested?  What are the advantages and disadvantages of tests using experiments?  using observations? 
  6. Briefly discuss three alternative explanations other than selection concerning trait s.
    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?
  7. Discuss the significance of wing waving in tephritid flies [Figs. 10.6 and 10.7 ] 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?
  8. Lizards and snakes were used as examples of observational studies of adaptation [Figs 10.9 , 10.10 , 10 .1 1 ].  
    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 10.1.
  9. 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?
  10. 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. 10.12 ]?  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. 10.15c] , does this change the conclusions?  Explain.
  11. What does figure 10.13 a purport to show?  What does figure 10.13 b show?  What is the significance of figure 10.13 c?   Discuss the significance of this figure to comparative studies of adaptation.  
  12. [Omit] What is meant by phenotypic plasticity?  Discuss the experiment using water fleas (Daphnia) to demonstrate this phenomenon.
  13. [OMIT] Discuss the evolutionary principles involved in the evolution of the mammalian middle ear.
  14. Regarding selection on female flower size in Begonia involucrata [Fig. 10.21 ]
    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? 
  15. 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?
  16. Regarding selection on flower color change in Fuchsia excorticata [Fig. 10.23 ]
    1. Explain what figure 10.23b 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. What are the benefits of this life history?  The costs?
    8. Is this an example of evolutionary tradeoffs or evolutionary constraints?  Explain.

Web Site Questions

  1. 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?
  2. 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 11 -- Sexual Selection  For all of your answers EXPLAIN fully with examples as needed. 

  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. How did Jones et al. [Fig. 11.5] evaluate the variation in reproductive success among male rough-skinned newts? Did males, or females, show greater variation in reproductive success? 
  6. What is the evidence that body sized in marine iguanas is controlled by stabilizing selection?  [see fig. 11.9b]
  7. 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?
  8. Explain the roles of natural selection and sexual selection in determining body size in marine iguanas (Fig. 11.9a).
  9. When and why can alternative mating strategies in male coho salmon be successful?
  10. Describe the experiment used by Gage to demonstrate sperm competition and ejaculate size in fruit flies.
  11. Why is infanticide a successful strategy for male lions and primates?  What is the advantage to females to spontaneously abort their young?
  12. What does figure 11.18 indicate about the costs and/or benefits of long versus short tails in male widowbirds
  13. How has female choice affected evolution of male long-tailed widow birds ? Discuss the experimental evidence that female choice drives sexual selection.  How do male widow bird s benefit from this?  Are there costs to the males?  How do female widowbirds benefit?  What is the experimental evidence for this?  How do females that pair with less desirable males increase their fitness?
  14. 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?
  15. What is the evidence that polyandry is quite common in female birds that used to be considered monogamous?
  16. What is the evidence that polyandry increases the fitness of  female prairie dogs?
  17. Discuss courtship and mating in hangingflies.  How do the males and females benefit from this behavior?
  18. Why is the size and quality of the food item presented by the male hangingfly (Fig. 11.24) important?
  19. Pipefish were cited as an example of an exception that can prove the rules of sexual selection.  Fully explain why.
  20. How can sexual selection explain why humans are sexually dimorphic?  Give examples.
  21. What evidence (from the Yanomamo, Poland, and pilots) suggests that female choice drives human sexual dimorphism?

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 12 -- Kin Selection  For all of your answers EXPLAIN fully with examples as needed. 

  1. Why did Darwin write that altruism posed a "special difficulty" to evolution by natural selection?
  2. What is Hamilton's rule?  How does it explain the evolution of altruism?
  3. What is the coefficient of relatedness and why is it important?
  4. Define and explain the significance of inclusive fitness.  
  5. What is direct fitness?  Indirect fitness?
  6. How can altruism spread when direct fitness is diminished?
  7. 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
  8. Explain alarm calling in Beldings ground squirrel in terms of kin selection.  Why is whistling considered selfish behavior and trilling altrusistic?
  9. How does the presence or absence of kin affect alarm calling in prairie dogs?
    1. Fully explain Figure 12.2b
    2. Fully explain Figure 12.2c
  10. How and why do male prairie dogs change their alarm calling behavior as they mature (Fig. 12.3)?
  11. Using Figs. 12.6 and 12.7, discuss the evolution of nest helping in white-fronted bee-eaters in terms of Hamilton's rule.  
    1. Fully explain Figure 12.6
    2. Fully explain Figure 12.7
  12. 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?
  13. Discuss kin recognition and how it is used in house mice to increase their inclusive fitness.
  14. How are house mice able to determine which newborns to nurse in communal nests?  What is the advantage of this behavior?
  15. What are altruistic sperm?  Why did they evolve?
  16. [not discussed 2008] What is the evolutionary significance of being a "clever coot"?
  17. Why does haplodiploidy produce unusual coefficients of relationships (Fig. 11.12).
  18. What is haplodiploidy?  How has it been used to explain the evolution of eusociality?
  19. Discuss the coefficients of relationship among parents, offspring, and siblings in haplodiploid insects
  20. Why doesn't haplodiploidy explain the evolution of eusociality in insects?   Give three reasons.
  21. Fully explain what the phylogeny of the hymenoptera explains about the evolution of eusociality (Figure 12.13)
  22. Why is inbreeding considered to promote eusociality?  How does inbreeding affect the direct and indirect fitness of members of a eusocial colony.
  23. Why are ecological factors as, or more, important than inbreeding as a selective agent in promoting eusociality?
  24. 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?
  25. Why are naked mole rats considered to be eusocial?
  26. Why conditions have led to the evolution of eusociality in naked mole-rats?
  27. [not discussed 2008] How does parent-offspring conflict affect direct and indirect fitness of parent and offspring?
  28. [not discussed 2008] 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?
  29. 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?
  30. 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. Explain fully the direct and indirect fitness costs and benefits.

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 14 -- Evolution and Human Health  For all of your answers EXPLAIN fully with examples as needed. 

  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 the flu virus to change genetically?
  6. What is function of hemagglutinin in the flu virus?  What is the significance of its antigenic sites?
  7. Explain Figure 14.5 a.  How does it provide evidence for the role of genetic drift in the evolution of the flu virus?
  8. Explain Figure 14.5 b.  Why are most of the flu strains dead ends?  What characterizes the successful strains that are ancestral to Wyoming '87?
  9. What is the evidence that natural selection is more important than drift in hemagglutinin evolution in the flu virus?
  10. What is the evidence for positive selection in the Influenza A virus.  Why is this knowledge of biomedical importance?
  11. Which flu lineages are most likely to survive from year to year?  What accounts for their success?
  12. What is the evidence for gene swapping in 1968 flu pandemic?
  13. Why is the Influenza A virus such a potentially lethal pathogen?
  14. What likely caused the global flu pandemic of 1968?
  15. 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? .
  16. What causes antibiotic resistance in pathogens?
  17. Why has reduced antibiotic use led to decreased pathogen resistance in some pathogens? (e.g., fig.14.11)
  18. Why are there costs to evolve antibiotic resistance?
  19. [Not discussed 2009] Discuss the significance of the experiment by Shragg et al. (Fig. 14.12)
    1. What strain (resistant/non-resistant) is most successful in the short term?  Why?
    2. What strain (resistant/non-resistant) is most successful in the long term?  Why?
  20. Discuss the three hypotheses have been proposed to explain the evolution of virulence .  Explain the role of natural selection in these processes.
    1. What is the coincidental evolution hypothesis to explain the evolution of virulence ?  Give an example.
    2. What is the short-sighted evolution hypothesis to explain the evolution of virulence ?  Give an example.
    3. What is the trade-off hypothesis to explain the evolution of virulence ?  Give an example.
  21. Use the transmission rate hypothesis to explain the virulence of HIV-1.
  22. [Not discussed 2009] Discuss the experiment of Messenger et al. ( Fig. 14.14 ) that demonstrated the relationship of phage virulence to length of vertical transmission period.
  23. Why are viruses that have more opportunities for horizontal transmission more virulent than those that have fewer?
  24. Why are vectorborne pathogens more virulent than those that are transmitted directly? (e.g., Fig. 14.15)   Explain the role of natural selection in this process.
  25. Discuss the evolution of virulence in intestinal bacteria as a function of the tendency toward waterborne transmission (Fig. 14.16).  Explain the role of natural selection in this process.
  26. 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?
  27. Discuss the evidence that myopia is maladaptive only in our present environment.   Explain the role of natural selection in this process.
  28. [not discussed 2008] Is fever adaptive in ectotherms?   What is the evidence?
  29. [not discussed 2008] Is fever adaptive in humans?   What is the evidence?
  30. What is the evidence that breast cancer can be virally induced?
  31. 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?
  32. [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 16 -- Mechanisms of Speciation.  For all of your answers EXPLAIN fully with examples as needed. 

    1. Define, give examples of, and explain the evolutionary significance with regard to speciation of
      1. anagenesis (not discussed 2011)
      2. cladogenesis (not discussed 2011)
      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. Gondwanan distribution pattern
      12. polyploidy
      13. chromosomal fissions and fusions
      14. genetic drift
      15. natural selection
      16. sexual selection
      17. sympatric speciation
      18. assortative mating
      19. secondary contact
      20. hybridization
      21. reinforcement
      22. prezygotic isolating mechanisms
      23. postzygotic isolating mechanisms
    2. What are the advantages of the morphospecies concept?  The disadvantages?  
    3. What are the advantages of the biological species concept?  The disadvantages?  What does it have in common with other widely used species definitions?
    4. What is lateral gene transfer?  What problems does this pose for the biological species concept?  the phylogenetic (evolutionary) species concept?
    5. What are the advantages of the  phylogenetic (evolutionary) species concept?  The disadvantages?
    6. How has the use of the phylogenetic species concept when applied to elephants modified our understanding of elephant diversity?  Why is this important for conservation biology?
    7. [Older edition, not discussed 2011] 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. 
    8. What are the three steps involved in speciation?
    9. Explain and compare and contrast isolation by dispersal and isolation by vicariance.
    10. What is the difference between allopatric and sympatric speciation?   How are allopatric and sympatric speciation similar?
    11. Is isolation essential for speciation?  Discuss its role in allopatric and sympatric speciation.  How do vicariance and dispersal differ as mechanisms promoting isolation?
    12. How does Figure 16 .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 .
    13. Discuss the stages and mechanisms involved in the evolution of Caribbean and Pacific snapping shrimp. What is the evidence that supports this hypothesis.
    14. Explain the history o f Caribbean and Pacific snapping shrimp shown in Fig. 16.8.  What is the significance of the branching pattern .   How can this pattern be explained by geologic history.
    15. What is the evidence that changes in chromosome structure played an important role in the divergence of our human ancestors from our ape relatives?
    16. What are the three most important mechanisms for genetic divergence in the speciation process?  Which is the most important?  Why?  The least important?  Why?
    17. Why was drift once thought to be important for genetic divergence during speciation?  Why isn't drift likely to cause significant genetic divergence?
    18. Regarding Rhagoletis, the maggot fly.
      1. Are the flies that parasitize apples and hawthorns distinct races /species ? 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 alleles had to be modified for the switch from hawthornes to apples?  Why are hybrids between the apple/hawthorne races less fit than their parents?
      5. What conclusions about evolutionary processes can be drawn from this?
    19. How has sexual selection led to divergence in some species of fruit flies? (e.g., fig. 16.10)
    20. 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?
    21. Define the two major classes of reproductive barriers (hint: = prezygotic and postzygotic) between closely related species?  Discuss the major examples of each of the two.
    22. Discuss the reinforcement processes at work promoting the genetic divergence of maggot flies.
    23. Why does prezygotic isolation occur faster in sympatric species pairs than in allopatric species pairs?
    24. What conditions are needed for hybridization to create a new species?  Give an example.
    25. Discuss the traditional (e.g., Mayr) and current views of the degree of genetic differentiation required to isolate populations and create new species.  Give an example of the current interpretation.

    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?
    9. (not discussed 2011) 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. (not discussed 2011) Compare and contrast anagenesis (phyletic change) with cladogenesis. Which represents "true" speciation (i.e., produces an increase in the number of species)
    3. (not discussed 2011) 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. (Older edition, not discussed 2011) 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.

 


Chapter 19 -- Evolution and Development.  For all of your answers EXPLAIN fully with examples as needed. 

  1. Define, give examples of, and explain the evolutionary significance of
    1. Homeotic (Hox) gene
    2. Regulatory gene
    3. Structural gene
    4. Regulatory protein
    5. Transcription Factor

Web Site Questions 

  1. What category of genes are Hox genes?
  2. What do homeotic genes do?
  3. What is the significance that Hox genes contain a DNA binding domain?
  4. What is the relationship among Hox genes, transcription factors, and gene expression during development?
  5. How do Hox genes function and in how are they important for development?
  6. What is the evidence that they Hox genes have been important for the diversification of animal body plans?
  7. Is it legitimate to claim that changes in Hox gene number were correlated with increased morphological complexity during animal evolution?  Explain why or why not.  Use examples from vertebrate evolution.
  8. In what way are vertebrate eyes and insect eyes homologous? What is the evidence?
  9. What do we know about the evolution of Hox gene number and regulation in animal evolution?
  10. The initial pattern of development of lobe-finned fish lobes and tetrapod limbs is dependent on the timing of expression of  Hox genes.  Using the concept of Hox genes, explain the evolution of the vertebrate limb.
  11. What evidence suggests that Hox gene duplication and elaboration was a key innovation
  12. What is the difference between microevolution and macroevolution?


Chapter 20 -- Human Evolution.  For all of your answers EXPLAIN fully with examples as needed. 

  1. Why and how how did Linnaeus classify humans among the primates?  Why did this represent a significant breakthrough?
  2. Discuss Figure 20.2, Sarich and Wilson's phylogeny of the apes.  How did they determine the information shown, including the relationships among the primates and the divergence times?
  3. How and why did Ruvulo et al's phylogeny (Figure 20.4) improve on that of Sarich and Wilson?
  4. Why is the number of human chromosomes different from that of chimps and gorillas?  What is the evidence for this?
  5. How do creationists classify transitional fossils in the human fossil record?  Why is this ignoring evidence?
  6. The fossil human Ardipithecus ramidus was named Science magazine�s story of the year 2009. List the 3 most important reasons why this fossil is so significant.
  7. What are the differences between australopithecines and the earliest members of the genus Homo?
  8. What is the evidence that human evolution was not a "ladder-like" progression from more primitive to advanced forms (Figs. 20.15, 20.16)?
  9. What is the evidence that Neandertals are a subspecies of Homo sapiens?  that they are a distinct species?
  10. How do paleoanthropologists determine whether a fossil hominoid was bipedal or quadrupedal?
  11. What is the African replacement hypothesis for the origin of modern humans?  What is the evidence for this?
  12. What is the hybridization and assimilation hypothesis for the origin of modern humans?
  13. What is the significance of Figure 20.8 showing differences in gene expression of humans, chimps and rhesus monkeys?
  14. What is neoteny?  How is it used to explain the divergence of modern humans from their more ape-like ancestors?