Chapter 1
Chapter 2
Chapter 3
Chapter 4
Chapter 5
Chapter 6
Chapter 8
Chapter 7, Section 7.2
Chapter 12
Chapter 14
Chapter 16

Chapter 1.  The case for evolutionary thinking: Understanding HIV

1.  What is AIDS? What is HIV?

2.  Why the "retro" in the term "retrovirus"?

3.  The number of proteins that can be synthesized corresponds roughly to the number of genes.  Given this, how can HIV complete its life cycle with just nine genes?  It would seem that even a relatively simple "organism" like HIV would require many more proteins than nine!

4.  How do cells of the immune system recognize that something is foreign or "non-self"?

5.  How does one die of AIDS?

6.  Why does AZT not interfere with normal cellular transcription (i.e. DNA to RNA)?

7. Consider this:  An HIV-positive patient takes AZT, but stops after his population of virions becomes resistant.  Will his HIV population maintain its resistance to AZT after he is off that drug?

8.  Does AZT cause the mutations which result in HIV strains resistant to AZT?

9.  Explain why anti-viral drugs are especially likely to cause negative side-effects in the host (patient).

10.  In Fig. 1.6 HIV-1/U455 is closer to HIV-1/LAI than it is to HIV-1/ANT70.  What does this imply about the phylogenetic relationship among these three strains of HIV?

11.  Why do the authors talk about the development of anti-HIV vaccines in the same section as their discussion of the origin and evolution of imunodeficiency viruses?

12.  The Ewald transmission rate hypothesis could be correct or false (we don't know yet), but it is certainly testable.  Explain.
 

1.  Is evolution the only possible explanation for the presence of homology and of vestigial structures in nature? Is it the most parsimonious explanation?

2.  True or false:  The fact that the earth is very old was only established in this century as a result of radiometric dating.

3.  What is the difference between relative dating of rocks and absolute (radiometric) dating of rocks?

4.  Why was the theory of evolution difficult to accept for many people in the mid 19th century? (Or today, for that matter!)

5.  What is the developmental explanation of structural morphology?

6.  Bat wings and insect wings are only analogous, but human eyes and insect eyes may be homologous.  Explain, referring to Fig. 2.2

7.  Construct a "Darwinian scenario" to account for the evolutionary change shown in Fig. 2.7

8.  Explain how Hutton's conclusions in geology supported evolutionary theory.

9.  Why have the authors included Fig. 2.13 in this edition of their text?

10.  What does it mean, in an evolutionary sense, to say that species are "related"?

1.  Explain the difference between the definition of "fitness" in the contexts of evolutionary biology and exercise physiology.

2.  Cite some examples of adaptations, showing how they meet the definition on p. 48.

4.  Why do the authors admire the "testability" of the theory of natural selection?

5.  Why don't all the birds have the same size beak?  [Two possibilities].

6.  Indicate which of the following  human traits are "heritable" in the sense of this term as used in genetics and evolutionary biology: blood type, height, skin color, number of limbs, number of cervical vertebrae, language spoken, upper body strength.

7.  How would you determine if seed production (i.e., number of seeds produced per individual) is a heritable trait in ragweed plants?

8.  Why is it essential that there be an excess of offspring for natural selection to occur?

9.  Table 3.2 show that the mean finch beak size increased, and this is easily explained.  But why did mean wing length increase as well?

10.  The authors define "preadaptation" as the evolutionary conversion of  function (e.g. the Panda's "thumb"). Provide some additional examples of  this phenomenon.

11.  Does evolution always trend toward more advanced and complex life forms?

12.  Does natural selection always work for the "good of the species"?

13.  How do the critiques of natural selection offered by Darwin's scientific contemporaries differ from the critiques offered by present day Creationists?

1.  What is a new allele?  A new gene?  Explain the distinction.

2. Do all point mutations results in changes in protein function?  Explain.

3.  Why must a mutation occur in germ line cells for it to be heritable?  Contrast the germline/somatic cell line situation situation in animals and plants.

4.  Rank these consequences of mutations in order of increasing frequency and explain: deleterious, beneficial, neutral.

5.  Explain why mutation rates based on recording loss-of-function mutations tend to underestimate the genome-wide mutation rate.

6.  Could mutation rate be a species trait subject to natural selection?  Hint - try applying Darwin's four postulates.

7.  What is the most common mechanism of gene duplication?

8.  How can gene duplication result in the evolution of new genes and new proteins?

9.  Why do chromosomal inversions increase linkage?

10.  How can polyploidization in plant populations result in the formation of new species literally overnight?

12.  What does it mean to say that a population is "genetically variable"?

13.  How is genetic variation determined?  Explain how the technique used (protein electrophoresis or DNA sequencing) affects the estimate of genetic variation in a population.

14.  What is an allele frequency? Hint - follow the Delta32 example on 97-99.

Chapter 5. Mendelian genetics in populations I: Selection and mutation

1.  What is an allele frequency?  A genotype frequency?  How are these values determined?

2.  What are the two main conclusions of the Hardy-Weinberg model?

3.  How is the Hardy Weinberg model used in research in evolutionary biology?  Give an example.

4.  Who did the selection in the Cavenor and Clegg experiment with drosophila and alcohol-spiked food:  the investigators or "the environment"?

5.  What is the ultimate outcome of directional selection on allele frequencies?

6.  Referring to Fig. 5.10, explain what is meant by "strong" and "weak" selection and indicate how the strength of selection influences the rate of evolution.

7.  Apply the reasoning developed in your answer to the previous question to the HIV/Delta32 scenarios in Fig. 5.13

8.  What types of selection result in these outcomes: fixation of alleles, equilibrium frequency of alleles so that both persist in the population, loss of heterozygotes from the population.  Provide a real-life example of each.

9.  In the example of the left-handed and right-handed fish (research by Hori, pp. 138-140), why doesn't one form replace the other?

10.  Referring to  this example, our text claims (p. 139) that the frequency of the dominant right-handed allele should be about 0.3 and the frequency of the recessive left-handed allele should be about 0.7.  Show why this is so.  (Aaah, a genetics problem!)

11.  Why is mutation by itself generally not a "potent evolutionary force "?

11.  What does Fig. 5.24 (evolution of cell size in E. coli) have to say about mutations and evolution?

1.  On the Lake Erie islands shown in Fig. 6.6, natural selection favors unbanded snakes.  Yet banded snakes persist on the islands.  How can this be explained?

2.  Fig. 6.9 shows the combined effects of genetic drift and gene flow on genetic diversity on islands.  How did the investigators (Giles and Goudet) explain this pattern?

3.  "Drift results from the vagaries of sampling."  What does this mean?

4..  Looking at Fig. 6.13 describe how population size affects the outcome of genetic drift.

5.  Does genetic drift generally result in adaptation?

6.  Explain these terms: genetic drift, founder effect, bottleneck effect.

7.  What effect does inbreeding have on allele frequency?  On genotype frequency?

8.  Why can breeding cause inbreeding depression?  Does it always?

9.  Why is inbreeding depression in plants easier to detect in wild populations than in the greenhouse or experimental garden?

10.   Is inbreeding more likely in large populations or small populations?  Explain.

11.  Do the authors discuss the female-biased sex ratio of the malarial parasite in their section on inbreeding?

1. Define: sexual reproduction, asexual reproduction, parthenogenesis, cyclical parthenogenesis.
2. What does Maynard Smith's model predict would happen if a mutation resulting in asexual mutation arises in a sexual population?
3. Do such mutations occasionally arise?  How do you know?
4. What is genetic recombination?  How does it occur?
5. Fig. 7.15 illustrates Muller's ratchet.  Explain why drift tends to eliminate the classes with low numbers of deleterious mutations, but not the classes with high numbers of deleterious mutations.
6. Explain how the Andersson and Hughes experiment (they subject bacterial populations to bottlenecks) supports Muller's hypothesis.
7. Explain how the Lambert and Moran study (they compared mutation incidence in endosymbiotiv bacteria and free living bacteria) supports Muller's hypothesis.
8. The "obvious" benefit of sexual reproductiuon is that it increases variability of young.  Would this always be advantageous?
9. Which type of environmental stress is more likely to favor sexual reproduction: physical or biotic?
10. In Fig. 7.18, explain why the investigators think the regression (best-fit) line has a positive slope.

1. Can all of the forces of evolution (selection, mutation, migration, drift, inbreeding) cause adaptation to occur?  Why or why not?
2. Why is the usual explanation of the long neck of a giraffe problematic?  What does this tell us about adaptive explanations of species traits?
3. How are sexual selection and natural selection similar?  How do they differ?
4.  Explain why the desert iguana performance curves in Fig. 8.8 have the shape they do.
5. Explain why the data in Fig. 8.8 is insufficient to show that desert iguanas exhibit behavioral thermoregulation.
6. Why should garter snakes "prefer" rocks of medium thickness?  Do they?  (Compare Fig. 8.9, 8.10 and Table 8.2.)
7. Explain why the ability  of Daphnia magna (pp. 270-271)  to reproduce asexually makes this species ideal for studying phenotypic plasticity.
8. Explain how Fig. 8.25 (phototactic behavior in Daphnia) demonstrates that phenotypic plasticity can evolve as an adaptation.
9. Individuals of  Fuchsia excorticata have a trait which is apparently maladaptive:  they maintain flowers on the plant after they lose the ability to produce or receive pollen.  Fitness would be increased by dropping the flowers soon after they cease to be functional.  Why hasn't natural selection fixed this glitch?
10. Give some examples of situations where "trade-offs" prevent optimization of individual traits.  Try to think of examples not cited by the text or in lecture.

1.  List some problems with the biological species concept.

2.  List some problems with the morphological species concept.

3.  Explain why morphological discontinuities between species defined using the morphological species concept suggest that the species might also fit the biological species concept.

4.  Is the Red Wolf a "good" species?

5.  Why is isolation essential for speciation?

6.  Distinguish between dispersal and vicariance as mechanisms of isolation.

7.  How does the information in Figure 9.6 suggest that speciation in Hawaiian Drosophila is the result of "island hopping"?

8.  Explain the differences and similarities between allopatric and sympatric speciation.

9.  The authors suggest that we are catching the early stages of speciation in Rhagoletis.  The apple and hawthorn races may diverge into separate species.  Do you think that present day human "races" will diverge into separate species in the future?

10.  Explain how reduced hybrid vigor following secondary contact can result in "reinforcement" of speciation.

11.  Distinguish between pre-zygotic and post-zygotic isolation, giving examples of each.

12.  Explain how hybridization can produce new species.

13.  How do we know that the Rift Lake Cichlids represent a rapidly spectating fauna?

14.  List the main factors that have been proposed as causes of the high speciation rates of the Rift Lake Cichlids.

15.  Explain how the information in Figure 9.24 shows that bird species tend to be younger than reptile and amphibian species.

16.  Explain how the information in Figure 9.25 shows that mammals speciate at higher rates than bivalves (mollusks).

1.  Define "cenancestor".

2.  Of all the genes in existence, why choose the gene for small-unit rRNA to construct a phylogeny of all life?

3.  Compare the criteria used to establish classifications of life based on (a) two kingdoms, (b) five kingdoms, (c) the scheme in Figure 11.5

4.  What is the basis for believing that the cenancestor had (a) a DNA-based genome, (b) no membrane-bound organelles, (c) extensive metabolic capacities , (d) introns?

5.  List the three steps of the Oparin-Haldane model for the origin of life?

6.  When did the cenancestor live?  How do we know?

7.  Where did the first organic chemical come from?

8.  How can monomers be assembled into polymers in the absence of protein-based catalytic enzymes?

9.  Explain how the rRNA phylogeny supports the endosymbiotic theory of the origin of mitochondria and chloroplasts.

10.  On the "introns early" theory, explain why the cenancestor lost its introns.

11.  Describe the evidence in support of the "introns late" theory.

1.  Approximately when did the common ancestor of gorillas, chimpanzees and humans live?

2.  About how old are the oldest human fossils?  This is a trick question.

3.  If humans evolved from apes, why are there still apes?  This is a trick question, too.  Actually it's a stupid question, but deal with it!

4.  Describe the main differences between Australopithecus and Homo.  How are these genera separable from related primate genera?

5.  Describe the multiregional evolution model for the development of modern humans and describe the evidence in support of it.

6.  Describe the single origin model for the development of modern humans and describe the evidence in support of it.

7.  How do the data in Figures 14.16, 17, 18 help to distinguish between the two models of modern human origins?

7.  Explain how reduced resource density during the Miocene-Pliocene may have led to evolution of smaller group size in chimpanzee ancestors and bipedal locomotion in human ancestors.

8.  Why do we know so little about the development of language in our ancestors and related species?

9.   Our primate relatives (e.g. chimps and gorillas) seem to be smarter than they need to be in order to forage for food, avoid predation, and so forth.  So why are we anthropoids so smart?