1. Regurgitate the definition of evolution and make sure you understand the definitions of the terms we used in that definition.
2. What was Darwin's critical insight into the mode of operation of this "natural selection" idea? In other words, in which two ways did his idea of selection differ from the way others before him (and in his own time) had thought about it?
3. What do we mean when we speak of "hidden genetic variation" in the context of selection and evolution in polygenic traits?
4. Why was Castle's work so critical for Darwinian selection?
5. Differentiate catastrophism from uniformitarianism.
6. One of the earliest critical observations about the fossil record was that it possessed ordered layers (strata without vertebrates always lower than strata with vertebrates; strata without mammals always lower than strata with mammals, etc.). How might an advocate of catastrophism explain the layering of fossil formations?
7. Consider the statement "Natural selection is not evolution." What did the writer of this statement mean? In other words, why is the statement true?
8. Darwin's notion that selection worked on small differences among individuals was subjected to several strong criticisms. What were these criticisms? One of them still presents a dilemma that is not fully resolved even today--can you offer an idea about which it is?
9. What did Darwin's critics mean when they criticized his concept of natural selection as one that was unlikely to result in stable, sustainable change? What did they mean when they criticized his mechanism as one that was unlikely to produce much in the way of an effective change in a continuous character?
10. Lyell calculated extinction rates between strata and estimated that an enormous number of species, more than were then known ever to have existed, must have been present at any "one-time only" creation in order to account for the patterns in extinction rates. What are the alternative explanations?
11. What do we mean when we say that natural selection is not "progressive"?
12. What was the significance of faunal regions? How about the significance of finding that fossil marsupials existed only in the same general parts of the world as present marsupials? Did you read Chapter 2?
13. What was the significance of observing that populations of a species on an island were distinguished from populations on the mainland?
14. Misconceptions about heredity hindered scientific acceptance of Darwin's proposed mechanism of natural selection. Discuss at least two of those misconceptions and how they appeared, quite legitimately, to be irreconcilable with Darwin's mechanism of natural selection.
15. At the turn of the 20th Century, most scientists accepted the idea of evolution, but it was not the idea advanced by Darwin. How did the common notion of that time differ from what Darwin had proposed?

Questions About Part Two: The Agents of Evolution

16. Biologists who study comparative embryology (species comparisons, for example) feel that they have a lot to contribute to the study of evolution. Which might be their contributions?
17. What is the significance of homologies that are not analogies, and how might that significance be related to the idea that small changes in early development produce large differences among adult forms?
18. While on a sojourn in northern Mexico you visit several springs and see variations on a theme in the size and color of a particular fish species. At spring A you find that the fish reach maturity at 25 mm length and are light brown in color. At spring B you find that the fish reach maturity at 30 mm and are dark brown in color. At spring C you find that the fish reach maturity at 35 mm and are nearly black in color. The springs are identical with respect to temperature, food level, water chemistry, etc. While waiting to cross the border at McAllen, Texas, you are engaged in conversation by another returning American who, after hearing of your discoveries, asks the following questions to occupy time at the border crossing while you are being searched for contraband material:

1. Describe how pleiotropy might be responsible for the distribution of phenotypes in different locations.
2. Describe how linkage might be responsible for the distribution of phenotypes in different locations.
3. Your new friend knows of a fourth spring where the fish mature at 25 mm but are pale and cream colored. Describe how epistasis might be involved in accounting for the entire pattern.
4. Your conversation is overheard by another tourist who mentions a fifth spring in which the fish matured at 25 mm length but were black in color. Now, if you consider all five springs, is it more likely that linkage or pleiotropy is creating this pattern, or do you still have insufficient information to eliminate either explanation?

19. Consider our fish with the variable vertebral numbers again. We have a stock in which all fish have 18 vertebrae, and we know that we have only Ab and aB gametes in our stock.

1. Obviously D < 0 in our stock. Is the release of stored genetic variation possible only if D < 0 or can stored variation be released when D > 0?
2. If the two loci have a recombination fraction of 0.01, how many generations will it take before the absolute value of D is less than the recombination fraction?
3. We decide we like "mediocre" fish (with 18 vertebrae), and we will sterilize any fish that shows up in our colony with either more or fewer vertebrae. Will we have to check our stock every generation, or will there be a point at which we will no longer have to worry because it will be impossible (barring mutation) to get a fish with any number of vertebrae other than 18? Does your answer change as the recombination fraction between the loci changes?
4. Now let's assume we have a very large colony of fish with all vertebral numbers, that the two loci are indeed unlinked, and that D = 0. We still would rather have mediocre fish (with only 18 vertebrae), so we embark on our sterilization program again. After about five generations of this artificial selection, will D still be 0? If not, will it be positive or negative in sign?
5. Can you describe any way in which we could get a stock of fish in which most if not nearly all fish had 18 vertebrae but the colony had D > 0?

20. Let's look at the slug Mucosus nauseatus. There are three genotypes, and their mucus-secretion rates and relative frequencies are as follows:

A1A1     10 cc/day     0.64
A1A2     8 cc/day       0.16
A2A2     2 cc/day       0.20

1. Are the genotypes at the A locus at Hardy-Weinberg frequencies?
2. What is the genetic variance in mucus-secretion rate?
3. If the alleles at the A locus had the same frequencies as above but were at Hardy-Weinberg genotype frequencies, would the level of genetic variance be the same as, exceed, or be less than the level in our slug population?

21. Mutation rates are sufficiently low, per locus per gamete per generation, not to be a strong force in producing evolution. Yet a close personal friend of yours claims that in fact mutations are very common in natural populations and therefore mutation rates play a significant role in evolution. Resolve this paradox.
22. If the genotypes at two loci are each at Hardy-Weinberg equilibrium frequencies, can there be gametic disequilibrium between the loci? If two loci are in gametic equilibrium, can the genotypes not be in Hardy-Weinberg equilibrium?
23. Consider a population in which all males have the genotype "aa" and all females have the genotype "AA" at a diploid, autosomal locus. Males and females are equally common. How many generations will elapse before the Hardy-Weinberg equilibrium is reached at this locus if mating is random?
24. A critic of the role of population genetics in evolution once said that the discipline of population genetics was silly because all its practitioners thought of evolution as a process of replacing one bean with another, that is, all they cared about was exchanging one allele for another via gradual replacement, one locus at a time. Clearly this critic has misunderstood the role of population genetics. Why do we study changes in allele frequencies, and is it true that we only think about one locus at a time? Which phenomena require multilocus explanations?
25. An experimental population of barley (Hordeum vulgare) was established by intercrossing of 30 barley varieties from various parts of the world. Two loci (A and B) coding for esterases were examined at various times; two alleles (1 and 2) were present at each locus. The gametic frequencies in three different generations were as follows (several thousand gametes were examined in each generation):

Gamete Relative Frequencies

Generation     A1B1     A1B2     A2B1     A2B2
4                      0.354      0.256     0.387      0.003
14                    0.407      0.098     0.491      0.004
26                    0.453      0.076     0.452      0.019

1. Calculate the value of D for each of these three generations.
2. What process(es) is (are) likely to be responsible for changing the gametic disequilibrium as the generations proceed?
3. If these two loci were tightly linked, how would this linkage affect the change in D over generations?

26. Consider a population of sea urchins with the following relative frequencies of gamete genotypes at two loci:

Genotype             Relative Frequency
A1B1                    0.91
A1B2                    0.00
A2B1                    0.00
A2B2                    0.09

1. Calculate the initial value of D.
2. Assuming random mating, what will the genotypic frequencies equal in the next generation after these gametes unite?
3. If there in no linkage between the two loci (r = 0.5), what will the value of D equal in the fifth generation?
4. If the two loci are linked and r = 0.2, what will the value of D equal in the fifth generation?

27. In Shorthorn cattle, the genotype A1A1 is phenotypically red coat color, A1A2 is roan (a mixture of red and white), and A2A2 is white.

1. If 108 red, 48 white, and 144 roan animals were found in a sample of Shorthorns from the central valley of California, calculate the frequencies of the A1 and A2 alleles for this population.
2. Is this population in Hardy-Weinberg equilibrium for the coat color locus? Prove your answer mathematically.
3. If this population is completely panmictic, what would be the expected genotypic frequencies of the next generation?

28. Consider the following phenotypic trait values for a single locus with two alleles:

Population     A1A1     A1A2     A2A2
1                     2.0         1.5          1.0
2                     2.0         2.0          1.0
3                     1.0         2.0          1.0
4                     2.0         1.0          2.0
5                     2.0         1.7          1.0

Each population represents an example of a different genetic relationship between the two alleles. The examples are complete dominance of A1, partial dominance of A1, no dominance, underdominance, and overdominance. Identify, in each population, which genetic relationship between the two alleles is described by the above trait values.

29. Two loci govern the variation in shell diameter in a snail population. The average shell diameters and relative frequencies of each two-locus genotype are as follows:

Genotype ave.     Diameter      Relative freq.
A1A1/B1B1          6 mm             0.125
A1A1/B1B2          5 mm             0.030
A1A1/B2B2          4 mm             0.095
A1A2/B1B1          5 mm             0.250
A1A2/B1B2          4 mm             0.060
A1A2/B2B2          3 mm             0.190
A2A2/B1B1          4 mm             0.125
A2A2/B1B2          3 mm             0.030
A2A2/B2B2          2 mm             0.095

1. Define epistasis. Is there evidence for epistasis between the loci in determining shell size?
2. Are the genotypes at each locus at Hardy-Weinberg frequencies? Prove your answer mathematically for each locus.
3. Calculate the level of genetic variance VG.

Now consider another population of snails and shell diameter values for each genotype:    

4. Is there evidence for epistasis between the two loci in this population? Why or why not?
5. BONUS FOR THE TRULY DEDICATED: We mentioned that epistasis is the interaction between alleles at different loci (i.e. it is a property of alleles, not loci per se). So, in this case, which alleles are interacting epistatically, and what is their overall effect?

30. Most of the differences between maize and its wild progenitor, teosinte, can be attributed to the effects of only four genes. Nonetheless, these two plants have very different phenotypes. How might you resolve this paradox?
31. Mutations are clearly biased; certain specific mutations at a locus occur more often than others (e.g. pelage mutations in mammals). What might be the evolutionary significance of this phenomenon?
32. Mukai's famous "mutation accumulation experiment" indicated that deleterious mutations occurred at a rate of 0.5 per genome per generation. What might this result suggest about the rate at which neutral mutations appear? Can you link this result with Castle's results to draw some tentative conclusions about which factors are likely to govern the rate of evolution?
33. What do we mean, specifically, when we use the term "genotype-environment interaction"?
34. It is claimed that humans and chimpanzees share over 98% of their genes; nonetheless, these two species look remarkably different to me and have some very different physiological attributes. Can you resolve this paradox?
35. Consider the hypothesis that mutations occur randomly along the string of nucleotides within an exon in a eukaryotic gene. We would test this hypothesis, in principle, by examining the DNA sequences of descendents of a germ cell and performing some sort of statistical analysis on where the mutations occur. But suppose we could examine the DNA sequences only of zygotic cells and some mutations were lethal, which prevents us from even seeing those mutants (because their carriers never appear in our experimental group). Do these lethal mutants create a bias that impairs our ability to test the original hypothesis?
36. One often reads about mutations being "random." In what sense are mutations random, and in what sense are they not?
37. Through which mechanisms do entirely new genes appear to arise? Did you read Chapter 4? Remember there are several--answering this question requires more effort than first appearances might suggest.
38. Define natural selection and discuss why the concepts of selection and evolution are not tautological.
39. Define and distinguish directional, optimizing, and disruptive selection.
40. Let's play Jeopardy^TM. The answer is "Because mutations that are neutral in one generation or in one location can be beneficial or deleterious in another generation or location." What might the question be?
41. Is there any configuration of genotype relative frequencies at two loci, with two alleles per locus, that would NOT be in Hardy-Weinberg proportions but that would exhibit complete gametic equilbrium? If you can derive such a configuration, can you relate it to anything else we've discussed in any lecture in the course (or to anything you've read in the text)?