Evolution Midterm

Evolution by natural selection is the logical outcome of four facts

1) Individuals vary in most or all traits; (2) some of this variation is genetically based and can be passed on to offspring; (3) more offspring are born than can survive to breed, and of those that do breed, some are more successful than others; and (4) the individuals that reproduce the most are a nonrandom, or more fit, subset of the general population.

Describe three major hypotheses for why HIV is so highly lethal.

1- short sighted evolution: within each patient, competition between HIV virions results in evolution of HIV strains that are more aggressive, replicate more rapidly and can evade attack by the host's T cells. This evolution is not the virus' long term benefit; however, because it ultimately kills the host- and kills all virions within that host. 2- evolution for transmission to new hosts: traits such as high viral load that can cause high virulence may also allow HIV to spread to new hosts. 3- Host has not had time to "counter-evolve": HIV is a new disease for humans, and our species has not yet had time to evolve defenses. We are still within the first generation of humans to be exposed to HIV. In addition, the frequency of the CCR5 delta 32 (resistant) alleles is very low in the parts of the world where HIV infection rate is the highest.

In our discussion of Weis and Abrahamson's work on goldenrod galls (data plotted in Figure 9.28), we men- tioned that the researchers established that there is heri- table variation among flies in the size of the galls they induce. How do you think Weis and Abrahamson did this? Describe the necessary experiment in as much detail as possible.

A basic strategy in any assessment of heritability is simply to measure the trait in as many parents as possible and as many offspring as possible, and plot midparent versus midoffspring values. In this case, we could measure gall size of larva, then collect the emerging larvae, raise them to adulthood in captivity, let them breed, let the females lay their eggs in a new set of plants, and finally measure the size of the offspring's galls. If paternity turned out to be difficult to assess or control, it is possible to estimate heritability using just the mother's data (as in Figure 9.21). As in any heritability analysis, close attention must be paid to shared environmental effects and other possible confounding influences. A likely confounding variable here is the mother fly's choice of plant, since the plant's species, genotype and environment may each affect gall size.

Sequences are now available for both the human and the chimpanzee genomes. Outline how you would analyze homologous genes in the two spe- cies to determine which of the observed sequence differences result from drift and which result from selection.

A classic approach is to calculate the ratio of replacement, or non-synonomous, substitutions to silent, or synonymous, substitutions. A ratio greater than 1.0 indicates that selection has acted on that site. However, this is a conservative test. A more sensitive approach is possible with the McDonald-Kreitman test, which compares the same ratio within versus among species. (The M-K test is not concerned with whether a given ratio is greater or less than 1.0, but rather with whether one ratio is greater than another ratio.) An M-K test would require numerous sequences from individual humans and chimpanzees. The ratio (replacement substitutions / silent-site substitutions) would be calculated both for human-human comparisons, chimp-chimp comparisons, and finally, human-chimp comparisons. A higher ratio for the human-chimp comparison than for the within-species comparisons would indicate that positive selection had occurred.

If a gene gets retroduplicated, how can you distinguish the original gene from the copy?

A copy of a retro duplicated gene would lack introns.

Suppose that you are starting a long-term study of a population of annual, flowering plants isolated on a small island. Reading some recent papers has convinced you that global warming will probably cause long-term changes in the amount of rain the island receives. Out- line the observations and experiments you would need to do to document whether natural selection occurs in your study population over the course of your research. What traits would you measure, and why?

A first step would be to identify some traits that affect the plant's survival or reproduction if rainfall changes, such as drought tolerance or resistance to root rot. We would then want to measure current variability in those traits, carefully assess the heritability of that variation, and explore the genetic and developmental underpinnings of the traits as much as possible. Over time, we would measure survival and reproduction (seed set, pollinator visits) of all the plants on the island. We would, of course, measure changes in the amount of rainfall and also keep an eye on other environmental factors that might affect our results. Over many years, we would inspect our dataset to see if certain genotypes were changing in abundance due to differences in survival and reproduction, and if these changes can reasonably be linked to rainfall. In another words, we would try to document any adaptations that might have evolved in response to these environmental changes.

Consider the nucleotide sequence TGACTAACG- GCT. Transcribe this sequence into mRNA. Use the genetic code to translate it into a string of amino acids. Give an example of a point mutation, an insertion, a deletion, a frameshift mutation, a synonymous substi- tution, a nonsynonymous substitution, and a nonsense mutation. Which of your examples seem likely to dra- matically influence protein function? Which seem likely to have little effect? Why?

A point mutation, such as T to G in the DNA strand, gives CCU for the first codon and that would replace amino acid threonine with proline. An insertion or a deletion would cause a frame-shift. For example, a deletion in DNA: TGACTAACGGCT, leaves mRNA sequence as: ACGAUUGCCGA and the polypeptide would be: Threonine-Isoleucine-Cysteine. Duplication/insertion of a single base also causes a frameshift, since each codon has three bases. This also affects the rest of the sequence. If the polypeptide change remains the same due to a change where DNA has one base-pair change, yet same amino acid remains in its place, we use the term synonymous substitution. For example ACU codes for Threonine, but if there is a silent substitution of ACU to ACC, ACG or ACA, the amino acid will remain in its place. The protein will function the same, with such mutation. A silent site mutation does not change the amino acid specified by a codon; a replacement mutation does. If there is a substitution of one amino acid to another, due to the base-pair change in DNA and RNA, we use the term non-synonymous substitution. A nonsense mutation will bring a stop codon, instead of an amino acid. Example is UUA for Leucine, might become a stop codon with one base change (UGA). Nonsense mutations probably affect the carrier most dramatically, because they do not allow polypeptide chain to grow.

Suppose a silent mutation occurs in an exon that is part of the gene for TAS2R38 in a human. Has a new allele been created? Defend your answer.

A silent mutation in the gene for TAS2R38 in human would create a new allele, because the DNA sequence will be different, yet it might not have any phenotypic effects, if the amino acids that are responsible for tasting PTC remain the same.

What is an evolutionary trade-off? Why do they occur? Give two examples. How does the occurrence of trade- offs illuminate the general question of whether all traits are adaptive?

A trade-off is a situation in which an increase the fitness of one trait will inevitably lead to a decrease in fitness of another trait. This can occur due to developmental constraints, or simply because organisms have a limited pool of energy and cannot develop all traits to a maximum degree simultaneously. Examples include testis size versus brain size in bats, and flower size versus number of flowers in begonias. The occurrence of trade-offs demonstrates that a particular trait can be adaptive in one context, yet the same trait can be non-adaptive in a different context.

In horses, the basic color of the coat is governed by the E locus. EE and Ee horses can make black pigment, while ee horses are a reddish chestnut. A different locus, the R locus, can cause roan, a scattering of white hairs throughout the basic coat color. However, the roan al- lele has a serious drawback: RR embryos always die dur- ing fetal development. Rr embryos survive and are roan, while rr horses survive and are not roan. The E locus and the R locus are tightly linked. Suppose that several centuries ago, a Spanish galleon with a load of conquistadors' horses was shipwrecked by a large grassy island. Just by chance, the horses that sur- vived the shipwreck and swam to shore were 20 chestnut roans (eeRr) and 20 nonroan homozygous blacks (EErr). On the island, they interbred with each other and estab- lished a wild population. The island environment exerts no direct selection on either locus. a. What was D, the coefficient of linkage disequilibrium, in the initial population of 20 horses? Was the initial population in linkage equilibrium or not? If not, what chromosomal genotypes were underrepresented? b. Do you expect the frequency of the chestnut allele, e, to increase or decrease in the first crop of foals? Would your answer be different if the founding pop- ulation had been just 10 horses (5 of each color)? Ex- plain your reasoning. c. If you could travel to this island today, can you pre- dict what D would be now? Do you have predictions about whether more horses will be roan versus non- roan, or chestnut versus black? If not, explain what further information you would need.

A) D was initially: (0)(0.25) - (0.50)(0.25) = -0.125. The population was not in linkage equilibrium; there were no RE chromosomes (roan black), and too many rE chromosomes (non-roan black). B) The chestnut allele will probably decrease because half of the chestnut alleles in this population are linked to the R allele, which carries a selective disadvantage (RR foals die). However, random genetic drift might interfere with this process; 20 horses is a small population, particularly considering only some of them can be mares. If the population were even smaller (e.g., 10 horses), genetic drift would have even greater effects. C) We can predict that more horses will probably be non-roan than roan, because of the extreme fitness disadvantage of RR horses. However, we cannot predict exactly what D will be, because of genetic drift, unknown sex ratios, and non-random mating. As for black vs. chestnut, we would need to know how often crossing-over occurs between the R and E loci. If crossing-over never occurs, black will probably be more common than chestnut.

Discuss how each of the following recent develop- ments—resulting from improvements in medicine, technology, pubic health, and from evolution— may affect the frequency of alleles that cause cystic fibrosis (CF). a. Many women with CF now survive long enough to have children. (CF causes problems with re- productive ducts, but many CF women can bear children nonetheless. CF men are usually sterile.) b. Typhoid fever in developed nations has declined to very low levels since 1900. c. In some populations, couples planning to have children are now routinely screened for the most common CF alleles. d. Drug-resistant typhoid fever has recently ap- peared in several developing nations.

A) Increase in CF allele frequency, due to increased reproductive success. B) Decrease in CF allele frequency, due to reduced heterozygote superiority. C) Decrease in CF allele frequency, due to (voluntarily) decreased reproductive success. D) Increase in CF allele frequency, due to increased heterozygote superiority.

Name the phenomenon being described in each of these (hypothetical) examples, and describe how it is likely to affect allele frequencies in succeeding generations. a. A beetle species is introduced to an island cov- ered with dark basaltic rock. On this dark back- ground, dark beetles, TT or Tt, are much more resistant to predation than are light-colored bee- tles, tt. The dark beetles have a large selective advantage. Both alleles are relatively common in the group of beetles released on the new island. b. Another beetle population, this time consisting of mostly light beetles and just a few dark beetles, is introduced onto a different island with a mixed substrate of light sand, vegetation, and black ba- salt. On this island, dark beetles have only a small selective advantage. c. A coral-reef fish has two genetically determined types of male. One kind of male is much small- er than the other, and sneaks into larger males' nests to fertilize their females' eggs. When small males are rare, they have a selective advantage over large males. However, if there are too many small males, large males switch to a more aggres- sive strategy of nest defense, and small males lose their advantage. d. In a tropical plant, CC and Cc plants have red flowers and cc plants have yellow flowers. How- ever, Cc plants have defective flower develop- ment and produce very few flowers. e. In a species of bird, individuals with genotype MM are susceptible to avian malaria, Mm birds are resistant to avian malaria, and mm birds are resistant to avian malaria, but the mm birds are also vulnerable to avian pox.

A) Migration followed by natural selection. The frequency of the T allele is likely to increase rapidly. B) Migration followed by natural selection. The frequency of the T allele may increase, but only slowly, and perhaps not at all, due to the rarity of the T allele and the weakness of selection. C) Frequency-dependent selection. The frequency of small males is likely to gravitate toward a stable equilibrium frequency, at which small and large males have identical fitness. D) Underdominance. One allele will very likely go to fixation, and the other allele will be lost. Which allele is lost is likely to depend on where the initial allele frequencies are, relative to the unstable equilibrium point. E) Heterozygote superiority, or overdominance. The frequency of the m allele is likely to gravitate toward a stable equilibrium frequency.

Kerstin Johannesson and colleagues (1995) stud- ied two populations of a marine snail living in the intertidal zone on the shore of Ursholmen Island. Each year, the researchers determined the allele fre- quencies for the enzyme aspartate aminotransferase (don't worry about what this enzyme does). Their data are shown in the graphs in Figure 6.36. The first year of the study was 1987. In 1988, a bloom of toxic algae (tan bars) killed all of the snails in the intertidal zone across the entire island. That is why there are no data for 1988 and 1989. Although the snails living in the intertidal zone were extermi- nated by the bloom, snails of the same species living in the splash zone just above the intertidal survived unscathed. By 1990, the intertidal zone had been recolonized by splash-zone snails. Your challenge in this question is to develop a coherent explana- tion for the data in the graphs. In each part, be sure to name the evolutionary mechanism involved (se- lection, mutation, migration, or drift). a. Why was the frequency of the Aat120 allele higher in both populations in 1990 than it was in 1987? Name the evolutionary mechanism, and explain. b. Why did the allele frequency decline in both populations from 1990 through 1993? Name the evolutionary mechanism, and explain. c. Why are the curves traced by the 1990-1993 data for the two populations generally similar but not exactly identical? Name the evolution- ary mechanism, and explain. d. Predict what would happen to the allele frequen- cies if we followed these two populations for another 100 years (assuming there are no more toxic algal blooms). Explain your reasoning.

A) Migration from the splash-zone population. The splash-zone population apparently had a much higher frequency of the Aat120 allele than did the intertidal population. B) Natural selection. The frequency of the Aat120 allele declined over several generations toward the original frequency seen in the intertidal population, likely due to selective differences in the two environments. C) Genetic drift. Random events can cause random deviations in allele frequencies from the expected course of evolution. This effect is stronger in small populations. D) We can expect both populations to arrive at the allele frequencies seen in the original intertidal population, assuming selective pressures remain the same and there are no significantly interfering events (such as, say, pronounced genetic drift, or mutation that creates a third allele).

Imagine a population of pea plants that is in linkage equi- librium for two linked loci, flower color (P = purple, p = pink) and pollen shape (L = long, l = round). a. What sort of selection event would create linkage dis- equilibrium? For example, will selection at just one locus (e.g., all red-flowered plants die) create link- age disequilibrium? How about selection at two loci (e.g., red-flowered plants die, and long-pollen plants die)? How about selection on a certain combination of genotypes at two loci (e.g., only plants that are both red-flowered and have long pollen grains die)? b. Now imagine a population that is already in linkage disequilibrium for these two loci. Will selection for purple flowers affect evolution of pollen shape? How is your answer different from that to part a, and why?

A) Selection at just one locus will not cause linkage disequilibrium, but the selection at more than one locus can. (It doesn't matter whether it is two independent selection events affecting the two loci, or one selection event that focuses on a certain combination of alleles. Either way, certain multilocus genotypes will have an advantage over others.) B) Once the population is in linkage disequilbrium, selection at one locus will affect evolution at the other locus. Comparing to the answer above, we see that in linkage equilibrium, single-locus selection does not affect other loci; but in linkage disequilibrium, it does.

a. Describe, in your own words, the three major modes of selection and their general effects on population means and on population variation. b. Which mode of selection is at work on gall size of the gall-making flies?

A) Stabilizing selection occurs when individuals with average values of a trait have highest fitness. This tends to trim the tails off of the population distribution, reducing variation, but not changing the population mean. Directional selection occurs when a value to one side of the population average (higher or lower, but not both) has highest fitness. This trims one tail off the population distribution and expands the other tail, shifting the population mean. Variation tends to reduce (because one tail is trimmed off) but not very much (because the other tail tends to lengthen, depending on available genetic variation). Disruptive selection results when high and low values have greater fitness than the average value. This tends to split the population into two morphs (forms) and reduce frequencies of individuals with trait values near the center of the distribution, increasing variation but not changing the mean. B) Gall size is under stabilizing selection, which in this case is due to opposing directional selection from birds and parasitoid wasps. If parasitoid wasps vanished, gall-making flies would be under directional selection by birds only, and average gall size would be expected to decrease.

Degree of antisocial behavior is a quantitative trait in hu- man males. Avshalon Caspi and colleagues (2002) used data on several hundred men to investigate the relation- ship between antisocial behavior and two factors. The first factor was genotype at the locus that encodes the enzyme monoamine oxidase A (MAOA). MAOA acts in the brain, where it breaks down a variety of the neu- rotransmitters nerve cells use to communicate with each other. The gene for MAOA is located on the X chromo- some. Due to genetic differences in the gene's promoter, some men have low MAOA activity and others have high MAOA activity. The second factor was the experi- ence of maltreatment during childhood. Based on a va- riety of evidence, the researchers determined whether each man had experienced no maltreatment, probable maltreatment, or severe maltreatment. The data are sum- marized in Figure 9.34. a. Is the variation among men in antisocial behavior at least partly due to differences in genotype? Explain. b. Is the variation among men in antisocial behavior at least partly due to differences in environment? Ex- plain. c. Do men with different genotypes respond the same way to changes in the environment? Explain. d. Is antisocial behavior heritable? Explain. e. Do these data influence your opinion about how men who exhibit antisocial behavior should be treated and/or punished?

A) The figure shows that variation in antisocial behavior is correlated with differences in genotype. It is possible that the correlation is due to some other factor (for example, certain genotypes may be more common in certain ethnic groups, which may be exposed to certain environments). However, if we leave that possibility aside, we can tentatively conclude that MAOA genotype is associated with antisocial behavior. B) Yes, because different levels of childhood maltreatment (an environmental condition) are associated with different levels of antisocial behavior. If there were no effect of environment, both lines would have a slope of 0 (parallel to the x-axis). C) Men with different genotypes respond in the same direction: for men in both MAOA categories, increased maltreatment is associated with heightened antisocial behavior. However, the strength of this effect is different in the two groups. Men with the low MAOA activity genotype appear more strongly influenced by environment than are men with the high MAOA activity genotype. The line for men with low MAOA activity has a greater (steeper) slope than the line for men with high MAOA activity, indicating a stronger effect of the environment factor on the x-axis. D) Yes. This means simply that some of the variation in antisocial behavior is attributable to genotype. E) The answer to this question is left to the reader.

In mammals, sex is determined by the X and Y chromo- somes. Females are XX; males are XY. The Y chromo- some contains a gene that causes development of testes, which then causes the embryo to become male. The Y Redrawn from Kohn et al. (2000). chromosome does not undergo crossing over with the X during spermatogenesis in males, but the two X's cross over with each other during oogenesis in females. a. The Y chromosome is thought to have once been the same size as the large, fully functional X chromo- some. But during the evolution of the mammals, the Y chromosome seems to have accumulated an enor- mous number of deleterious mutations. It has also lost almost all of its genes and has shrunk to a rudimentary chromosome containing just the testis-determining gene, a few other genes, and some nonfunctional remnants of other genes. Why has this occurred? b. Birds use a reverse system, in which females have two different chromosomes (called WZ in birds) and males have two of the same kind of chromosome (ZZ). In birds, sex is determined by a gene on the W chromosome that causes ovary formation, which then causes the bird embryo to become female. Would you predict one of these chromosomes might have accumulated mutations in the same way that the Y chromosome has? If so, which one? c. Some plants also have genetically determined sex but are polyploid. Should their sex chromosomes show accumulation of mutations?

A) Y chromosomes never have an opportunity to cross over with another Y chromosome. Each Y chromosome is always the only Y chromosome in its cell. This means that, ironically, the very chromosome that causes sexual reproduction in mammals is itself vulnerable to the major disadvantage of asexual reproduction: lack of genetic recombination. The Y chromosome suffers from random accumulation of mutations due to Muller's ratchet, and also from selective sweeps of beneficial alleles that drag deleterious linked alleles along with them. B) In birds, the W chromosome never has an opportunity to exchange genes with any other W chromosomes. Like the Y in mammals, it is vulnerable to Muller's ratchet and selective sweeps, and has accumulated a large number of deleterious mutations. The same phenomenon has occurred in virtually all organisms that have sex chromosomes (except see below). C) Polyploidy allows the rarer sex chromosome to cross-over with the extra copies present in each cell. Because of this genetic recombination, the sex chromosomes in polyploid plant taxa are full-size, normal chromosomes and have not large numbers of deleterious mutations.

Now consider heritability in more general terms. Sup- pose heritability is extremely high for a certain trait in a certain population. a. First, can the trait be strongly affected by the environ- ment despite the high heritability value? To answer this question, suppose that all the individuals within a certain population have been exposed all their lives to the same level of a critical environmental factor. Will the heritability value reflect the fact that the environ- ment is very important? b. Second, can the heritability value change if the envi- ronment changes? To answer this question, imagine that the critical environmental factor changes such that different individuals are now exposed to different levels of this environmental factor. What happens to variation in the trait in the whole population? What happens to the heritability value?

A) Yes, the trait may be strongly affected by environment. But no matter how important the environment could potentially be, if there is little variation in environment, the heritability value will typically be very high. B) Heritability values will often change if the environment changes. Typically, if a formerly invariant environment begins to change, heritability values will decrease.

recycles the neurotransmitter serotonin after it has been used to carry a message between nerve cells in the brain. There are two alleles of the serotonin transporter gene: s and l. Klaus-Peter Lesch and colleagues (1996) found that people with genotypes ls and ss, score slightly, but significantly, higher than people with genotype ll on psychological tests of neuroticism (see Figure 9.35). a. Are these data consistent with the hypothesis that the serotonin transporter gene is a QTL that influences neuroticism? Explain. b. Is the serotonin transporter gene the gene for neuroti- cism? Explain. c. Can you think of another plausible explanation, in which the serotonin transporter gene plays no role at all in neuroticism? Explain.

A) Yes. A QTL, or quantitative trait locus, is any locus at which genetic variation in alleles is statistically associated with variation in a given quantitative trait. QTLs may be identified by various mapping techniques (generally, investigating large sections of the genome for markers that are statistically linked to the trait) or by investigation of particular loci that are already suspected to affect the trait. In this case, the serotonin transporter gene was suspected to affect neuroticism, since serotonin is a neurotransmitter known to affect mood. B) No. Like most quantitative traits, neuroticism is almost certainly influenced by many genes, only some of which have been discovered, and only some of which vary in genotype. (Variation in serotonin transporter genotype explains only about 5% of variation in neuroticism. Many other QTLs associated with neuroticism have since been found.) C) Several other explanations are possible. The serotonin transporter gene might be physically linked to another locus that affects neuroticism. The frequencies of s and l alleles might vary among different human populations, and those populations might differ in frequencies of other genes, or may be exposed to different environments.

What is an evolutionary constraint? Why do they occur? Give two examples. How does their occurrence illumi- nate the general question of whether all traits are adap- tive?

An evolutionary constraint is an obstacle that prevents a taxon from evolving a certain trait, often due to developmental pathways, or some other competing process of physiology or ecology. Examples include pigs' failure to evolve wings (due to a developmental program that does not allow multiple pairs of forelimbs), the retention of flowers on Kotukutuku trees for several days after fertilization (possibly due to the physiological constraint of slow growth of pollen tubes), and the lack of host shifts in body feather lice of birds (possibly due to an ecological constraint of limited dispersal opportunities). The occurrence of evolutionary constraints demonstrates that not all traits are perfectly adaptive.

Describe in your own words the difference between an experimental study, an observational study, and a com- parative study. What sorts of questions are they each suited for (i.e., why don't researchers always use the ex- perimental method)? Give an example of each type of study from this chapter.

An experimental study is one in which the researchers directly manipulate a variable of interest, typically changing it in one group of individuals and leaving it unchanged in a control group. The experimenters determine which individuals are assigned to each group. Examples include Hansen et al.'s nectar guide experiment, Weeks' oxpecker-exclusion experiment, and Greene et al.'s experiment on wing-waving in tephritid flies. Experimental studies are extremely powerful because they can control for other confounding variables, but not all questions can be studied this way, particularly those that involve large-scale evolutionary changes. An observational study is one in which researchers simply observe the patterns that occur in nature, such as Huey et al.'s study of rock selection in garter snakes. (Sometimes, observational studies may compare two groups of animals that occur in nature. However, the researchers do not assign individuals to the different groups; rather, the individuals have "assigned themselves" to the different groups, which can introduce considerable confounds.) A comparative study is one that compares different taxa of organisms, often studying the distribution of a trait on a phylogeny, and seeking to understand why some clades evolved the trait and others did not. Examples include Hosken's study of testis size in bats, and Futuyma et al.'s study of host shifts in leaf beetles. A comparative approach is very useful when many taxa have evolved a similar trait. Frequently, the overall research plan will include a combination of several of these different approaches.

Black color in horses is governed primarily by a recessive allele at the A locus. AA and Aa horses are nonblack colors such as bay, while aa horses are black all over. (Other loci can override the effect of the A locus, but we will ignore that complication.) In an online conversation, one person asked why there are relatively few black horses of the Arabian breed. One response was, "Black is a rare color be- cause it is recessive. More Arabians are bay or gray because those colors are dominant." Discuss the merits and/or problems with this argument. (As- sume that the A and a alleles are in Hardy-Wein- berg equilibrium, which was probably true at the time of this discussion.) Generally, what does the Hardy-Weinberg model show us about the impact that an allele's dominance or recessiveness has on its frequency?

An important lesson of Hardy-Weinberg equilibrium is that recessiveness and dominance, by themselves, cannot cause allele frequencies to change. Intuitively, many people expect that dominant alleles will tend to become more common, simply because of their dominance, but this is not so. In horses, some other breeds are entirely black (e.g., Friesians), demonstrating that recessiveness alone should not prevent black from being a common coat color. Black color has been historically rare in Arabians, perhaps originally because of natural selection against dark (hot) coat colors in this ancient desert-adapted breed and later because the color was not selected by Arabian breeders. In the last two decades, black Arabians have become more common in the United States because Arabian breeders began selecting for this color after the movie The Black Stallionmade black Arabians fashionable. Thus, selection by horse breeders has begun to reverse the effects of a much older period of natural selection in a desert environment.

As we have seen, inbreeding can reduce offspring fitness by exposing deleterious recessive alleles. However, some animal breeders practice genera- tions of careful inbreeding within a family, or "line breeding," and surprisingly many of the line-bred Chapter 7 Mendelian Genetics in Populations II: Migration, Drift, and Nonrandom Mating 287 animals, from champion dogs to prize cows, have normal health and fertility. How can it be pos- sible to continue inbreeding for many generations without experiencing inbreeding depression due to recessive alleles? (Hint: Consider some of the dif- ferences between animal breeders and natural selec- tion in the wild.) Generally, if a small population continues to inbreed for many generations, what will happen to the frequency of the deleterious re- cessive alleles over time?

Animal breeders have an advantage over natural selection-they can assess the likely future consequences of their actions, and can alter their selection plans accordingly. "Line breeding" is usually successful only when careful animal breeders deliberately avoid breeding any individuals suspected to carry deleterious recessive traits or reduced fertility. In addition, line-bred animals typically have good veterinary care, which may reduce effects of inbreeding depression due to reduced heterozygosity (i.e., reduced resistance to new diseases). In general, if an inbred population can survive the first several generations of inbreeding (when deleterious alleles are first exposed), the frequency of deleterious alleles will eventually decline as natural selection weeds them out. (Deleterious alleles are not the only problem of inbreeding, however. A longer-lasting problem may be the reduction in allelic diversity.)

How do chromosome inversions happen? What conse- quences do they have for the evolution of populations?

Chromosome inversions result from two breaks in DNA, a flipping of the broken segment, and then annealing of the segment at the breakpoints. Inversions might lock certain allele combinations that are advantageous for a population. Such adaptive frequency variations of some inversion types had been documented in many Drosophila studies.

What is codon bias? Why is the observation of non- random codon use evidence that certain codons might be favored by natural selection? If you were given a series of gene sequences from the human genome, how would you determine whether co- don usage is random or nonrandom?

Codon bias is the over-representation of a particular codon for a given amino acid in a genetic sequence, relative to other synonymous codons. Neutral molecular evolution should produce sequences that use an equal mix of all available synonymous codons for a given amino acid; therefore, when codon bias occurs, it is likely the result of selection. A simple test for codon bias in a given sequence is to calculate the frequency of each codon relative to the frequency of synonymous codons. As illustrated by the results in Figure 7.24, these calculations should be done separately for each gene, or family of genes, as there may be interesting codon-bias differences across different types of genetic sequences.

In the mid-1980s, conservation biologists reluc- tantly recommended that zoos should not try to preserve captive populations of all the endangered species of large cats. For example, some biologists recommended ceasing efforts to breed the ex- tremely rare Asian lion, the beautiful species seen in Chinese artwork. In place of the Asian lion, the biologists recommended increasing the captive populations of other endangered cats, such as the Siberian tiger and Amur leopard. By reducing the number of species kept in captivity, the biologists hoped to increase the captive population size of each species to several hundred, preferably at least 500. Why did the conservation biologists think that this was so important as to be worth the risk of los- ing the Asian lion forever?

Conservation biologists were hoping to keep the captive population size (for each species) high enough to avoid loss of allelic diversity and inbreeding depression. Ultimately they were trying to minimize the risk of extinction of the captive populations, over a time scale of up to several centuries into the future. As of a 2009 report , the Felid Taxon Advisory Group of North American Zoos is now attempting to manage 16 species of large cat, almost all of them endangered, in an estimated 2,100 available zoo living spaces. The Asian lion was indeed phased out, partly due to the fact that the entire captive population was discovered to be descended from hybrid Asian-African lions.

Conservation managers often try to purchase corri- dors of undeveloped habitat so that larger preserves are linked into networks. Why? What genetic goals do you think the conservation managers are aiming to accomplish?

Corridors can potentially link small isolated populations together, causing increased gene flow among them, and reducing the effects of genetic drift. The intended genetic goals are the preservation of allelic diversity and increased heterozygosity.

Darwin maintained that among living species, there is no such thing as a higher (more evolved) or lower (less evolved) animal or plant. Explain what he meant.

Darwin believed that evolution by natural selection must be a branching process, and not a linear or progressive process. There are lineages that appeared earlier in evolution and thus are considered more basal relative to lineages that appeared later and are considered more derived, but no species is any higher or lower than any other.

List the sources of evidence that were available to Darwin and those that appeared later. For example, of the evidence for microevolution discussed in section 2.1 Darwin knew, and wrote about divergent strains of domestic plants and animals and about vestigal structures. However, in Darwin's day no one had ever directly observed change across generations in natural populations. For each section, indicate which evidence you consider strongest and which you considered weakest. Explain why.

Darwin was aware of the following: -Vestigal structures -Geological evidence for mass extinctions -succession in the fossil record -Structural and developmental homologies -The evidence from biogeography based on occurrence of closely related species in groups of islands -The age of earth known to be much greater than previously believed to be Much significant evidence came after darwin: -Mendel's research and concept of genes -Transition fossil forms -Direct observation of population in the wild changing through time -Genetic and molecular information of any kind, including vestigial molecular traits, molecular homolgies and basic genetics -Radiometric dating and absolute dates for the geologic time scale

Figures 2.20 through 2.22 show examples of transitional fossils. If Darwin's theory of evolution is correct, and all organisms are descended with modification from a common ancestor, predict some other examples of tran- sitional forms that should have existed and that might have produced fossils. If such fossils are someday found, will that strengthen the hypothesis that such transitional species once existed? Conversely, if such fossils have not been found, does this weaken the hypothesis that the transitional species once existed?

Darwin's theory of evolution has a good base in the fossil record. The fossil record is a case of "absence of evidence is not evidence of absence." Many species do not leave any discoverable fossils at all, due to such factors as our lack of access to deeply buried strata and the complete destruction of large sections of the earth's crust in subduction zones. Thus, presence of a fossil obviously proves that the predicted species once existed, but absence of known fossils does not prove that it did not exist.

For which of the following studies would you recom- mend the use of Felsenstein's method of phylogeneti- cally independent contrasts? Why? a. A comparison of feather parasite burden and beak shape in different species of birds. b. An experiment that tests whether birds whose beak shapes are experimentally altered will end up with greater parasite loads (similar to Clayton et al.'s study). c. An observational study that measures the correla- tions among beak shape of individual birds with their preening behavior, and with their parasite loads.

Felsenstein's method is useful for case A, but not for the other two studies. Felsenstein's method was designed to test questions in comparative studies only, particularly those that involve comparisons of quantitative traits, (e.g., testis size and group size in bats). Felsenstein's method is a method for controlling for phylogenetic relatedness, which otherwise can add a major confounding factor to comparative studies.

Some physicians have advocated "drug holidays" as a way of helping HIV patients cope with the side effects of multidrug therapy. Under this plan, every so often the patient would stop taking drugs for a while. From an evolutionary perspective, does this seem like a good idea or a bad idea?

From an evolutionary perspective, this is a risky idea. Recall HIV's high mutation rate and large population size. A break in multiple drug therapy allows the surviving HIV virions- most of which will be those with partial resistance to one or two of the drugs- to multiply and generate billions of offspring with new mutations, some of which will confer mutations to additional drugs. However. a break in the therapy might promote an increase in the frequency of "wild type" or non-resistant virions too, which could lead to a more effective treatment.

What were Futuyma and colleagues' two hypotheses to explain why leaf beetles have not colonized all possible species of host plants? What did the researchers do to test the hypotheses? How do their results illuminate the general question of whether all traits in all organisms are adaptive?

Futuyma et al.'s two hypotheses were: 1) all host shifts are possible, and ecological factors and random chance are the only factors that determine which host shifts actually occur; and 2) not all host shifts are possible, because the beetles lack genetic variation to eat certain species of host plants. Futuyma et al. tested the hypotheses by using quantitative genetic trait analysis. They examined the genetic variation associated with four of the beetle species' ability to survive (or not) on six of the possible hosts. They found that, in fact, not all host shifts are possible - that is, these four beetle species often lacked the necessary genetic variation to detoxify the leaf toxins in different plant species. Futuyma et al.'s results show that some traits (in this case, the trait of only eating the leaves of one host plant species) may not be adaptive, or not entirely adaptive; they may simply reflect an evolutionary constraint due to lack of genetic variation.

Diagram two processes through which genes can be du- plicated. How can you tell whether a duplicate copy of a gene arose by unequal crossing over or retroposition

Gene duplication is very common. See Figure 5. 26. The ones that arose from unequal crossing over—homologous chromosomes aligning incorrectly—would be close by (in a tandem) and contain the same introns as their parental genes. The ones that arose through retrotransposition would first of all lack introns (RNA is copied back to DNA) and they would be scattered far away from the original gene.

Bodmer and McKie (1995) review several cases, similar to achromatopsia in the Pingelapese, in which genetic diseases occur at unusually high frequency in populations that are, or once were, relatively isolated. An enzyme deficiency called hereditary tyrosinemia, for example, occurs at an unusually high rate in the Chicoutimi region north of Quebec City in Canada. A condition called por- phyria is unusually common in South Africans of Dutch descent. Why are genetic diseases so com- mon in isolated populations? What else do these populations all have in common?

Genetic diseases are common in isolated populations due to founder effects and subsequent genetic drift. These random effects can, just by chance, override the effects of selection, sometimes resulting in deleterious alleles becoming quite common. These effects are much more pronounced in small populations; the three populations mentioned here are all quite small.

What is the difference between genetic variation, en- vironmental variation, and genotype-by-environment interaction? Give examples of each.

Genetic variation is based on differences in alleles (versions of a gene) and ultimately the entire genomes, among the individuals. Genetic variation is necessary for evolution, since these differences are encoded and transmitted from one generation to the next. For example, genetic variation in a blood type gene in humans, results in four different phenotypes. In this case, three different alleles of one gene are: I A, I B, i (where I A and IB are codominant, while allele i is recessive to either one). Different combinations of these alleles produce four possible phenotypes: A, B, AB and O blood types, with different frequencies in different parts of the world. Environmental variation is based on the differences produced when same genotypes are exposed to different environments. This usually happens because certain environments might alter gene expression. For example one genotype in a species of plants, often produces different sizes of mature plants, when grown in the different altitudes or with different soil nutrients. Similarly, dark pigmentation on the tips of ears and paws of Siamese cats develops in certain latitudes with colder temperatures. Many additional examples of traits that could vary a great deal under environmental changes are found in quantitative traits. Genotype by environment variation is based on both differences in the genomes and ways that environment affects the phenotypes. When one genotype develops different phenotypes in different environments, we could say that this genotype exhibits phenotypic plasticity. For example, a change from asexual to sexual reproduction, based on the amount of nutrients, predation or parasitism. Phenotypic plasticity can also evolve.

Review the process by which the HIV population inside a human host evolves resistance to the drug AZT. What traits of HIV contribute to its rapid evolution? How might a similar scenario explain the evolution of antibiotic resistance in a population of bacteria?

HIV has a very high mutation rate, a rapid reproductive rate and an enormous population size. This means that at any given time, a human infected with HIV is carrying tens of millions of HIV virions with millions of different random mutations. Inevitably, a mutation will occur that confers resistance to AZT. This will typically be a mutation that causes greater selectivity in the active site of the reverse transcriptase enzyme. Notice that the HIV population has heritable variation for resistance to AZT before exposure to AZT. However, at this stage the resistance to AZT occurs only in one or a few virions out of the billions. In other example of this type of evolution, such as in the evolution of microbial resistance to antibiotics, we expect similar outcomes. It would take longer for the evolution of the resistant strains of bacteria, when compared to evolution of the HIV virions, which might happen within an individual patient. However, bacteria easily share their antibiotic resistance genes with other bacteria via conjugation and other forms of lateral genetics exchange. The main difference will be in the specific nature of the mutation- it will not occur in the gene for reverse transcriptase, but in some bacterial gene.

When did HIV enter the human population, and from what source? How do we know?

HIV is a new disease for humans and it probably came to the human population from a simian host (SIV strain). The genetic sequence data indicates that the last common ancestor of the M HIV-1 viruses lived in the 1930's or earlier. This strain is primarily responsible for the AIDS epidemic. The key to HIV's rapid evolution is a very high mutation rate, an extremely fast reproductive rate and a very large population size within one host. This makes it virtually inevitable that at least one HIV virion within one patient will, by chance, acquire a key mutation that will cause increased replication or resistance.

Suppose you are telling your roommate that you learned in biology class that within any given human population, height is highly heritable. Your roommate, who is study- ing nutrition, says, "That doesn't make sense, because just a few centuries ago most people were shorter than they are now, clearly because of diet. If most variation in human height is due to genes, how could diet make such a big difference?" Your roommate is obviously correct that poor diet can dramatically affect height. How do you explain this apparent paradox to your roommate?

High heritability within a population does not mean that variation between populations is due to genetic differences. If the populations differ in an environmental factor, the variation between populations can be due entirely to environment. In this case, your roommate is comparing height between two populations (a medieval population versus a modern population) that differ in dietary environment.

High-crowned teeth that are well suited for grazing are found in some rodents, rabbits and hares, most even- toed hoofed animals, horses (which are perissodactyls), and elephants. According to the evolutionary tree in Figure 4.37, are high-crowned teeth a synapomorphy or a product of convergent evolution?

Homology in high-crowned teeth can be claimed if traits have a similar genetic and developmental basis, or if a large number of other traits also link the species in question. However, this does not seem to be the case in the diverse lineages from Figure 4.37. Thus, in the case of the mammalian evolutionary history, high crowned teeth are probably the result of convergent evolution.

What is homoplasy? Why does homoplasy make it more challenging to estimate evolutionary history?

Homoplasy is defined as a similarity in traits that is not due to inheritance (not derived) from a common ancestor. Homoplasy is misleading because it makes species that are not closely related appear as if they are closely related. If the genetic and developmental basis of a morphological trait is known, then researchers can distinguish homology from homoplasy. Morphological traits can also be measured in fossil species. Compared to morphological traits, DNA sequence data are relatively easy to acquire in large amounts, but can be subject to extensive homoplasy.

A clade in a phylogeny bears a label at its base giving a bootstrap support of 97%. What does this mean?

If a clade in phylogeny has a 97% bootstrap support, there is strong evidence (97%) that a clade of interest belongs to a monophyletic group where this estimate was found. The phylogeny is positively evaluated using the bootstrapping method.

Think about how the finch bill data demonstrate Dar- win's postulates. a. What would Figure 3.10 have looked like if bill depth was not variable?

If bill depth was not variable, Figure 3.10 would show one skinny, high bar—all finches would have had exactly the same bill depth.

If Darwin's four postulates are true for a given popu- lation, is there any way that evolution cannot hap- pen? What does this imply about whether evolution is or is not occurring in most populations today?

If the four postulates are true, a population is virtually certain to evolve unless selection is extremely weak and genetic drift is very strong. Since the four postulates are almost always true, virtually all populations of organisms are evolving today, at least with regard to some genetic loci.

What would Figure 3.15 look like if bill depth was variable but the variation was not heritable?

If the variation in bill depth was not heritable, the two graphs in Figure 3.15 would look the same. The 1978 post-drought birds would still have the same average bill depth as the 1976 birds (even though the 1978 chicks had thicker-billed parents). The population would not have evolved.

Describe the three mathematical consequences of link- age equilibrium. That is, what three equations about genotype and chromosome frequencies will be true if a population is in linkage equilibrium? What is D, and how is it calculated?

If two loci, A and B, are in linkage equilibrium: The frequency of any particular allele at one locus does not vary with the alleles present at the other locus, The frequency of any chromosome haplotype can be calculated by multiplying the frequencies of the separate alleles, and: D, the coefficient of linkage disequilibrium, is zero. D is calculated as: gABgab = gAbgaB, where gAB is the frequency of chromosomes carrying alleles A and B, and so on.

In Figure 3.11, why is the line drawn from 1978 data, after the drought, higher on the vertical axis than the line drawn from 1976 data, before the drought?

In Figure 3.11, there is a strong correlation between midparent beak depth and the midoffspring beak depth. Parents with a given average bill depth had slightly thicker-billed chicks in 1978 than in 1976. Such a trend demonstrates heritability of beak depth and suggests that some alleles tend to produce shallow beaks, while other alleles produce deeper beaks. There is also probably a slight environmental effect on beak depth too.

Design a study to test our prediction that human populations will evolve in response to selection imposed by HIV.

In africa, the disease is so widespread and so clearly affects reproductive success that it appears likely that humans will evolve in response to HIV. This would be a good place to conduct such a study. Wherever you conduct a study, you could start with identifying individuals who were exposed to HIV but not infected. You could also search for people who remain healthy despite being infected. In both cases, you would search for a genetic/molecular basis of their resistance to HIV.

Referring to the information in Figure 4.10, explain why the bones found in bird wings and bat wings are homologous. Then explain why the use of the forelimb for powered flight is a convergent trait in birds and bats

In the Figure 4.10 we see major monophyletic groups of tetrapod vertebrates. The arrangement of bones in the forelimbs is ultimately homologous among all tetrapods, because all tetrapods have similar components. However, bats are descendants of tetrapod mammal ancestors whose forelimbs were used for walking. The bat wing is morphologically very different form a bird wing and thus, an analogous structure. This is because birds are descended from dinosaurs. The ability to fly evolved independently in the two vertebrate groups.

Consider a population containing the following geno- types: Aa, Aa, AA, aA, aa, Aa, aa, aA, aa, Aa. What is the frequency of genotype aa? Allele A? Allele a? Can you tell which genotype is most advantageous? Can you tell whether Aa resembles AA or aa? Why or why not?

In this population, the allele frequency of allele "a" or "f (a)" will be: (2x 3) + 6/ (2x10) = 12/20 = 0.6 f (A) = 0.4 Since we only have 10 individuals (genotypes) in the population, we cannot make good conclusions about the advantageous genotypes. If we had a larger sample, in the similar ratios: 6Aa: 3aa: 1AA, we could say that heterozygotes are the most advantageous. If we use symbols A and a, we are indicating that allele A is dominant over a. Thus we have two phenotypes in our population of 10 individuals, where dominant phenotype A/- is represented with 7 individuals, while recessive phenotype aa is represented with 3 individuals.

If you were a manager charged with conserving the collared lizards of the Ozarks, one of your tasks might be to reintroduce the lizards into glades in which they have gone extinct. When reintroducing lizards to a glade, you will have a choice between using only individuals from a single extant glade population or from several extant glade populations. What would be the evolutionary consequences of each choice, for both the donor and recipient pop- ulations? Which strategy will you follow, and why?

Introductions from a single population will reduce the population size of the donor population. The resulting recipient population is likely to have low allelic diversity and low heterozygosity (at most equal to, but most likely lower than, the source population). However, this strategy might also preserve unique genotypes of the source population. Introductions from several donor populations will have a lower impact on the size of each donor population, and the resulting recipient population will likely have greater allelic diversity and higher heterozygosity than any of the source populations. However, this strategy may result in loss of unique genotypes and loss of any adaptations that the various donor populations had evolved to their particular environments. The choice of strategy is up to the reader.

In 1992, Spolsky, Phillips, and Uzzell reported genetic evidence that asexually reproducing lineages of a sala- mander species have persisted for about 5 million years. Is this surprising? Why or why not? Speculate about what sort of environment these asexual salamanders live in, and whether their population sizes are typically small (say, less than 100) or large (say, more than 1,000).

It is surprising because sexual reproduction usually has an advantage over the long term, due to changes in selection (parasites, changing environment, etc.) and Muller's ratchet (especially in small populations). We can predict that these asexual salamanders live in stable environments in large populations.

This researcher proposes that natural selection on hu- mans favors individuals who die relatively early in life. His logic is that the trait of dying from VNTR mutations is beneficial and should spread because the population as a whole becomes younger and healthier as a result. Can this hypothesis be true, given that selection acts on indi- viduals? Explain.

Krontiris is referring to the evolution and trade-offs in life history traits in humans. Natural selection typically eliminates traits that are detrimental to the individual carrying the trait. Even if others in the group would benefit, such a trait affecting longevity would be eliminated from the population. However, if short longevity is associated with higher reproductive rates or earlier sexual maturity, evolution would favor (positive selection) these VNTR mutations. This research is also referring to group selection in humans. In this case, selection of the trait is detrimental to the individual carrying the trait but is favorable to other members in the group. When the individual in question is closely related to other members of the group, this is a possible outcome (kin selection), yet group selection theory is frequently supported in research.

How can you identify an allele that has experienced re- cent strong positive selection?

Loci that have been under recent positive selection will usually be in linkage disequilibrium with nearby neutral markers (indicate an allele of young age), and will be at relatively high frequency for the allele's age.

A common creationist criticism of the finch study is, "But it's just a little change in beak shape. Nothing really new has evolved." Or put a different way, "It's just mi- croevolution and not macroevolution." The finch team continues to spend a great deal of effort on their proj- ect—traveling thousands of miles to the remote Galápa- gos every year, just to try to band an entire population of birds and all their nestlings and measure their bills. How would you respond to the creationists' criticisms? Do you think the ongoing 30-year-effort of the finch bill project has been worthwhile? Is it useful to try to document microevolution, and does it tell us anything about how macroevolution might work?

Many answers are possible. Though it may be "just" microevolution, the shape of a bird's bill is not a minor feature for the bird—it is the bird's one and only food-handling tool. Furthermore, microevolution and macroevolution are not a dichotomy—macroevolution is simply microevolution carried out for a long time. The changes that most laypeople would consider "macroevolution" typically require hundreds of thousands of years to evolve, so it is not logical to expect to observe them in a single field study. Evolutionary biologists generally regard long-term studies of microevolution as highly informative for learning how natural selection happens in a natural environment, and for a close-up look at the causes of small changes that, eventually, can add up to macroevolution.

Allele age and linkage disequilibrium

Measurements of linkage disequilibrium are useful in inferring the history of alleles. If an allele is in linkage disequilibrium with nearby neutral marker loci, we can infer that the allele is relatively young. If we have an es- timate of the rate at which disequilibrium between the allele and the nearby neutral marker loci breaks down, then we can use the strength of the persisting disequi- librium to estimate the allele's age. If an allele is both young, as indicated by linkage disequilibrium, and pres- ent at high frequency, then we can infer that the allele has recently been favored by positive natural selection.

In Muehlenbachs et al.'s study of placental malaria, why was it important that they studied infants born during both high and low malaria season? Can you think of any other possible explanations for their data?

Measuring genotype frequencies during the low malaria season provides a control because it demonstrates that in the absence of natural selection by malaria, genotype frequencies are close to Hardy-Weinberg equilibrium. This provides a basis for comparison with the results from the high malaria season, in which genotype frequencies deviate significantly from equilibrium, indicating that one of the assumptions of Hardy-Weinberg is not true during this season. One alternative explanation (others are possible) is that seasons influence the sexual behavior of men and women in Tanzania in a way that results in non-random mating with respect to the VEGFR1 locus during the months of September through January (nine months before the high-malaria season infants are born), but random mating with respect to the same locus during other months of the year. This would require that a person's VEGFR1 genotype correlates with sexual behavior that is also influenced by the time of year.

Discuss factors that might cause mutation rates to vary among individuals in populations, and among species.

Mutation rates vary among loci in one genome, among different individuals and among different species and taxa. In general mutation rates vary among individuals because the enzymes responsible for copying and repairing DNA vary in accuracy. Mutation rates vary among species because trade-offs occur between the speed and accuracy of copying and repairing DNA, and because higher or lower mutation rates may increase fitness in certain environments.

The idea behind multidrug therapy for HIV is to increase the number of mutations required for resistance and thus reduce genetic variation in the viral population for survivial in the presence of drugs. Could be achieve the same effect by using antiretroviral drugs in sequence instead of simultaneously?

No, we could not achieve the same result if we administer the drugs in a sequence. The unfortunate result would likely be development of resistance to all the drugs. This is because the HIV population would only have to develop resistance for one drug at a time, which is quite easy for it to do. The key to multiple drug therapy is that the drugs are given simultaneously, so that HIV virions must have four or five simultaneous mutations (one for each drug) to survive. Even with HIV's high mutation rate and large population size, the simultaneous occurrence of multiple resistance mutations in one virion is unlikely.

Diagram the sequence of events that leads to the forma- tion of second-generation polyploid individuals in plants that can self-fertilize.

Plants can become polyploid in several ways, but if polyploidy results from one original species (not the hybrids) the following steps might be involved: If a mutation occurs leading to diploid gametes and this individual self-fertilize, the offspring would be a tetraploid (4n), which would either backcross to a parent like plant or cross with a similar plant from the same species. The unequal number of chromosomes in the gametes from polyploidy species and gametes from normal diploid plants would probably result in the reproductive isolation. Thus a tetraploid species might evolve further differences.

Compare and contrast the evolutionary roles of point mutations, chromosome inversions, gene duplications, and polyploidization.

Point mutations affect a single point (base-pair) in a DNA sequence. They could be: transitions (replace a purine with a purine or a pyrimidine with a pyrimidine), transversions (replace a purine with a pyrimidine or a pyrimidine with a purine), as well as deletions or duplications of a single base pair. They are an important source of genetic variability and in most cases have some effect on fitness. On the contrary, large scale mutations (chromosomal structure changes), such as inversions, duplications, translocations and deletions; affect larger portions off genome and they have more drastic effects on phenotypes, as well as on fitness. In addition, they could be associated with divergent populations. Polyploidy refers to multiplication of the entire genomes/chromosomal sets (chromosomal number changes). This could often lead to speciation.

Recall that the fourth chromosome of Drosophila melanogaster does not recombine during meiosis. The lack of genetic polymorphism on this chromo- some has been interpreted as the product of a selec- tive sweep. If the fourth chromosome had normal rates of recombination, would you expect the level of polymorphism to be different? Why?

Polymorphism would be much higher on the fourth chromosome if recombination could occur. Recombination would have broken the physical linkage between whatever gene was experiencing positive selection, and all other genes on the chromosome. This would have allowed other genes on the chromosome to maintain allelic diversity even while one allele at the selected locus was moving to fixation.

What are reaction norms, and why do they matter? Draw your own reaction norm for mood as a function of the temperature outside. What kind of variation allows reaction norms to evolve?

Reaction norm is a pattern of phenotypes one individual might develop when exposed to varying environments. Different genotypes would show different mood change/reaction to changing temperatures.

In this chapter we saw that in many cases, gene fre- quencies in small populations change at different rates than in large populations. As a review, state how the following processes tend to vary in speed and effects in small versus large populations. (As- sume the typical relationship of population size and generation time.) Selection Migration Genetic drift Inbreeding New mutations per individual New mutations per generation in the whole pop- ulation Substitution of a new mutation for an old allele Fixation of a new mutation

Selection: Lesser effects in small populations, due to the greater impact of genetic drift Migration: Greater effects in small populations, because each new migrant represents a greater proportion of total population size Genetic drift: Greater effects in small populations Inbreeding: Greater effects in small populations New mutations per individual: Similar in populations of all sizes New mutations per generation in the whole population: Fewer in small populations New mutations per year in the whole population: Fewer in small populations Probability that a new mutation will be effectively neutral: Similar in populations of all sizes Neutral mutation rate: Similar in populations of all sizes

When researchers compare a gene in closely related species, why is it logical to infer that positive natu- ral selection has taken place if replacement substitu- tions outnumber silent substitutions?

Silent substitutions accumulate at a rate determined largely by mutation rate and genetic drift. If replacement substitutions accumulate at a faster rate than silent substitutions, some other process must be driving new alleles to fixation faster than genetic drift could do alone. This process is likely to be natural selection: There are other processes that could affect fixation rate, but they are unlikely to vary between replacement sites and silent sites.

Researchers began to find AZT resistant strains of HIV 1 in recently infected patients who had never received AZT. How can this be?

Since an HIV population already has heritable variation for resistance to AZT before exposure to AZT, some patients would quickly develop resistant HIV strains as soon as they began taking AZT/ Although early application of AZT in the 1990s showed some success in preventing or slowing replication of most HIV virions, the resistant virions with the right mutation would survive and replicate. In more general terms, there is a differential reproductive success among the virions that is linked with a heritable trait, such as AZT resistance.

By using the start codon AUG as a guidepost, re- searchers can determine whether substitutions in pseudogenes correspond to silent changes or re- placement changes. In contrast to most other loci, the rate of silent and replacement changes is identi- cal in pseudogenes. Explain this observation in light of the neutral theory of evolution.

Since pseudogenes are noncoding, mutations at "replacement" sites in pseudogenes do not actually result in an amino acid replacement. Thus the "replacement" mutations, like silent-site mutations, are neutral, and are not affected by natural selection.

Consider the hypothesis that disease causing agents naturally evolve into more benign forms as the immune system of their hosts evolve more efficient responses to them. Is the evidence we have reviewed on the evolution of HIV within and among hosts consistent with this hypothesis? Why or why not?

So far, HIV has shown no tendency to evolve into a more benign form. Within one host, HIV almost always evolves to become more virulent, as demonstrated by the multiple studies reviewed in this chapter on AZT resistance, epitope evolution, replicative speed, etc. Across hosts, the form of HIV that has spread most widely is the more virulent one, HIV-1. It appears that the same traits that cause increased virulence might also cause increased transmission to new hosts. A virus must only keep its host alive long enough to spread to a new host; once it spreads, it doesn't matter (for the virus's continued survival) if the first host dies.

Consider the experiment described in Section 2.1 in which Ted Garland and colleagues bred mice to run long distances on exercise wheels. We presented the re- sults as evidence that two dozen generations of selec- tive breeding had altered the experimental population. How does the control strain support this interpretation? If Garland had simply compared the behavior of the 24th experimental generation to the behavior of the first experimental generation, would the evidence for evolu- tion be as strong? Explain

Strong evidence of evolution is seen in the results that come from selective breeding. In the experiment, microevolution could be observed after only 24 generations of selection. The experimental design and procedure was designed to measure the effect of selection and the change of the population. From a larger population of mice, the researchers chose high runner lines and control lines, each with 10 mated pairs. They needed to keep track of each generation in the experiment because they selected a male and female which run the greatest distance, to produce the next generation. On the contrary, the control strains had male and female pairs chosen at random in each generation. Female mice from the selected lineages ran almost three times faster than the control mice. This is direct evidence that population and species change over time.

Populations of rats exposed to the poison warfarin rap- idly evolve resistance. The gene for warfarin resistance is located on rat chromosome 1. Michael Kohn and col- leagues (2000) surveyed rats in five German rat popula- tions known to vary in their recent exposure to warfarin and in their resistance. The researchers determined the genotype of each rat at a number of marker loci near the warfarin resistance gene. For each population, the researchers calculated the average heterozygosity (H) among the marker loci, the fraction of loci that were out of Hardy-Weinberg equilibrium (HWE), and the fraction of marker-locus pairs that were in linkage dis- equilibrium (LD). Their results appear in Figure 8.32. Based on these graphs, rank the five populations in or- der, from lowest to highest, for exposure to warfarin and resistance. Explain your reasoning.

Strong positive selection tends to cause high linkage disequilibrium and tends to lower heterozygosity. Therefore we can deduce that the x-axis must start with low resistance on the left, and go to high resistance on the right. The most resistant population should be WU, and the least resistant should be LH This deduction is correct: the most resistant rat population is WU, followed by BK, PS, HT, and LH. In the original graphs, the x-axis goes from 0% resistance on the left to 100% resistance on the right.

What is a synapomorphy

Synapomorphy is a characteristic that is shared by two or more species and also derived. This means that it was modified in a common ancestor and then inherited by the descendant species.

An owner of racing greyhounds asks you how she can identify some of the loci and alleles that distinguish win- ners from losers. Describe, in as much detail as possible, a research program that might reveal this information.

The breeders wish to identify QTLs associated with race performance. Many different research programs are possible. In general, we would analyze genetic samples from as many greyhounds as possible (winners and losers), for as many genetic markers as possible. We would then look for statistical associations between presence of each genetic marker and race performance. Performance could be measured in several ways: winning of stakes races, fastest recorded times of certain distances (regardless of whether they won), siring offspring that raced well, etc. Alternatively, we might also investigate candidate loci that are already suspected to contribute to performance, such as loci known to contribute to endurance, muscle contraction speed, aerobic capacity, and bone density.

According to the text, it is correct to claim that most finches died from starvation during the 1977 drought because "there was a strong correspondence between population size and seed availability." Do you accept this hypothesis? If so, why don't the data in Figure 3.13 show a perfect correspondence between when seed supply started falling and when population size started to drop?

The claim that the vanished finches probably died of starvation is certainly reasonable given the data in Figure 3.13 and the absence of obvious other causes such as increased predation or disease. The graphs in Figure 3.13 show that most small, soft seeds disappeared between about July and October of 1976, the same time that the bird population began to decline. Seeds were still abundant at first, but they were predominantly large seeds. Then, even the large seeds began disappearing, and the bird population continued to decline sharply. The birds did not all die instantaneously because it takes time for an animal to starve to death, and some individuals were likely able to scratch for the few remaining small seeds for several months before succumbing to starvation.

What is the difference between a molecular phylogeny reconstructed by parsimony versus maximum likelihood?

The difference between a molecular phylogeny reconstructed by parsimony and/or by maximum likelihood methods is the way we evaluate evolutionary trees of the taxa—clades—we are studying. When we evaluate the trees based on the minimum number of evolutionary steps (changes), we say that we are looking for the most parsimonious tree. If we are looking for the probability that any given phylogenetic tree offers the best estimate of evolutionary history for the taxa we are studying, we use maximum likelihood statistics.

Which kind of mutation is most common: lethal, non- lethal but deleterious, neutral, or beneficial? Draw a graph to illustrate your answer. According to the graph, do most mutations have large or small effects on fitness?

The effect of mutations on fitness could be: deleterious, lethal or beneficial. Many mutations do not have effect on fitness and we could consider them neutral. Lethal and deleterious mutations are much more common than beneficial.

In everyday English, the word adaptation means an ad- justment to environmental conditions. How is the evo- lutionary definition of adaptation different from the everyday English sense?

The everyday meaning of "adaptation" refers to a change that occurs in a single individual's lifetime, while the evolutionary meaning refers to a trait that has developed via natural selection over many generations. An evolutionary adaptation is also defined strictly in terms of relative reproductive fitness, while the everyday meaning can refer to changes that do not necessarily affect reproduction.

In an editoral published on March 28, 2009, the Lancet quoted Benedict XVI on Africa's battle with HIV/AIDS. The problem, the Pope said, "can't be overcome by the distribution of condoms. On the contrary they increase it." Not surprisingly, this statement generated some controversy. Consider the relevant scientific evidence. Is the Pope's first statement correct. How about his second statement? How do we know?

The first statement is true in that no single strategy will prevent the transmittal of HIV/AIDS. For instance, condoms provide some protection from sexually transmission of HIV/AIDS, but they would not prevent an infected mother from passing the virus to her babies via breast milk. The Pope's second statement is that the distribution of condoms actually increases the problem of HIV/AIDS transmission. Disagree because data collected in South Africa shows that consistent use of condoms reduces HIV infection significantly.

List the five conditions that must be true for a population to be in Hardy-Weinberg equilibrium. Why is it useful to know the conditions that pre- vent evolution? For each condition, specify wheth- er violation of that assumption results in changes in genotype frequencies, allele frequencies, or both.

The five conditions are: no selection, no mutation, no migration, no chance events (also can be stated as infinite population size, or no genetic drift), and random mating. Violation of selection, mutation, migration, and/or chance events will result in changes in allele frequencies and genotype frequencies in the population. Violation of random mating—but not the others—will result in changes in genotype frequencies but not in allele frequencies.

Describe Darwin's four postulates in your own words. What would have happened in the snapdrag- on experiment if any of the four had not been true?

The four postulates are, briefly: variation exists, the variation is heritable, survival and reproduction are not equal, and survival and reproduction are not random. In the snapdragon experiment, if there had been no variation, all flowers would have been the same color. If variation had not been heritable, the colors of the best-reproducing plants would not have been passed to their offspring. If there had not been unequal survival and reproduction, all plants would have attracted equal numbers of bees and produced equal numbers of seeds. If survival and reproduction had been random, some plants would have had more bee visits and produced more seeds than other plants, but the difference would not be related to plant color. In any of these four cases, the snapdragon population would not have evolved.

The transitional fossils in Figure 2.21 demonstrate that dinosaurs evolved feathers long before they evolved flight. Clearly, feathers did not evolve for their aero- dynamic advantages. What else, besides aerodynamics, do feathers do for birds today? What advantages might feathers have offered for dinosaurs? Can you think of a way to test your hypothesis?

The original advantage of feathers might not be related to flight. Birds are endothermic ("warm-blooded"), and their body feathers are critically important as insulation. Feather coloration is also important in species and sex recognition, and feathers are frequently used in behavioral displays. Any of these functions may have played a role in the feathered dinosaurs, with insulation generally suspected to have been particularly important. Mathematical models of the thickness and potential value of the dinosaur feathers, as well as close inspection of other anatomical and locomotory features associated with endothermy, could clarify whether the dinosaurs' feathers had a thermoregulatory benefit. In addition, feathers might also play a role in sexual selection, as it is the case in modern birds.

Given the risk of evolution of resistance, why do you think the two patients were not given high doses of AZT immediately rather than starting them with low doses?

The patients were probably not given higher doses because of the serious side effects of antiviral drugs. Since viruses use their host cell's molecular machinery, any drug that can stop viral replication usually interferes with normal healthy cells as well. AZT can disrupt cell division because it interferes with DNA transcription in healthy cells, not just HIV infected cells.

Consider three facts: (i) Loss of heterozygosity may be especially detrimental at MHC loci, because allelic variability at these loci enhances disease re- sistance; (ii) Microsatellite loci show that the gray wolves on Isle Royale, Michigan, are highly in- bred (Wayne et al. 1991); (iii) This wolf popula- tion crashed during an outbreak of canine parvo- virus during the 1980s. How might these facts be linked? What other hypotheses could explain the data? How could you test your ideas?

The population crash of the Isle Royale wolves may have been related to low heterozygosity at MHC loci, and consequently lowered disease resistance, in the small population. Another possible explanation is that parvovirus could have caused a massive crash in any population of wolves, regardless of their MHC heterozygosity. (Canine parvovirus appeared suddenly in 1978, apparently derived from a mutant feline distemper virus, and spread worldwide in just a few months. Mortality rates exceeded 80% in many canid populations.) The two hypotheses could be tested by comparing MHC heterozygosity and parvovirus resistance of this wolf population to other, more outbred, wolf populations. If parvovirus mortality rate is related to MHC heterozygosity, wolf populations that are more outbred should have showed lower mortality than the Isle Royale wolves during the parvovirus outbreak.

Why was it important that G. H. Hardy used vari- ables in his mathematical treatment of changes in population allele frequencies across generations? Would it have been equally useful to simply work several more examples with different specific allele frequencies?

The use of variables allowed Hardy to prove the general case: that—given the five assumptions—any allele frequencies will stay in equilibrium. Before this proof, it was not intuitively clear to most people that the specific allele frequencies did not matter. As is often the case, general proofs expressed mathematically can reveal important patterns that were not always intuitively obvious beforehand.

Given the strength of selection that bumblebees exert on alpine skypilots, why haven't flower corollas in the tundra population evolved to be even larger than they are now? Develop at least two hypotheses, and describe how you could you test your ideas.

There are several possibilities. Alpine skypilots may still be evolving larger size; bumblebees may prefer a certain size of flower, but not the largest sizes; or there might be opposing forces of selection in the tundra that limit large flower size. The first possibility could be tested by monitoring skypilot flower size over several generations; the second by testing bumblebee preference for flowers of many sizes, possibly including artificially enlarged flowers (e.g., attaching extra petals to existing flowers); and the third by measuring fitness in an experimental tundra population that is hand-pollinated instead of bumblebee-pollinated, to see if larger flowers have any disadvantages. Many variations of each of these experiments are possible.

In humans, the COL1A1 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 risk of fractures in both Ss and ss women. A study of 1,778 women showed that 1,194 were SS, 526 were Ss, and 58 were ss (Uitterlinden et al. 1998). Are these two alleles in Hardy-Weinberg equilibrium in this population? How do you know? What information would you need to determine whether the alleles will be in Hardy-Weinberg equilibrium in the next generation?

These alleles appear to be in Hardy-Weinberg equilibrium. Expected genotype frequencies (calculated as p2, 2pq, and q2, where p=0.82 and q=0.18) match observed frequencies (SS=0.67, Ss=0.30, ss=0.03) almost perfectly. To assess whether the alleles will stay in Hardy-Weinberg equilibrium, we would need to know whether selection, migration, mutation, random events, and nonrandom mating are likely to be major factors. In this particular case, the possible selective disadvantage of the recessive s allele is the most obvious factor. It would be useful to know the severity of bone fractures and the age at which they tend to occur, and, especially, whether they substantially affect an Ss or ss child's health or survival or a grown Ss/ss woman's likelihood of having children.

We used Figure 6.14 as an example of how the fre- quency of an allele (in fruit flies) does not change in unselected (control) populations but does change in response to selection. However, look again at the unselected control lines in Figure 6.14. The fre- quency of the allele in the two control populations did change a little, moving up and down over time. Which assumption of the Hardy-Weinberg model is most probably being violated? If this experiment were repeated, what change in experimental design would reduce this deviation from Hardy-Weinberg equilibrium?

These small changes are likely due to genetic drift caused by chance events. The easiest way to reduce this effect is to use a larger population size. This topic is discussed further in Chapter 7.

Describe the major hypotheses for the cause of high frequency of the CCR5@∆32 allele among European populations. Why is the age of the allele relevant for dis- tinguishing among the hypotheses? Do we know how old this allele is, and if so, what is the evidence?

This allele is thought to have risen to relatively high frequency due to either selection or genetic drift. Genetic drift tends to work more slowly than strong selection. If the allele arose recently, selection is the most likely factor, but if it arose long ago, genetic drift could have brought it to high frequency. Early studies indicated that the allele arose about 700 years ago. Since this is quite recent, it suggested that selection due to a historically recent epidemic (the Black Death or smallpox) might have driven the allele to high frequency. More recent studies based on improved chromosome maps have estimated an age of 5000 years ago, and the allele has actually been recovered from Bronze Age skeletons, proving that the allele is at least several thousand years old. This suggests that genetic drift may have played a role, but selection was likely involved as well.

The amino acid sequences encoded by the red and green visual pigment genes found in humans are 96% identical (Nathans et al. 1986). These two genes are found close together on the X chromosome, while the gene for the blue pigment is located on chromosome 7. Among pri- mates, only Old World monkeys, the great apes, and hu- mans have a third pigment gene—New World monkeys have only one X-linked pigment gene. Comment on the following three hypotheses: • One of the two visual pigment loci on the X chromo- some originated in a gene duplication event. • The gene duplication event occurred after New World and Old World monkeys had diverged from a common ancestor, which had two visual pigment genes. • Human males with a mutated form of the red or green pigment gene experience the same color vision of our male primate ancestors.

This hypothesis is logical, because the genes are located in tandem, they have high sequence similarity, and more basal groups (New World monkeys) have only one X-linked pigment gene. This hypothesis is also logical, because all of the lineages in the Old World have two pigment genes on the X chromosome, while all of the lineages in the New World have only one. If a human male has a knock-out mutation in the gene for one of the X-linked pigment genes, then that individual cannot make red or green pigment. That person's vision would be more similar to ancestral primates or New World monkeys than to other humans.

"Natural selection no longer influences mankind to any great extent." Do you agree? What is your evidence?

This is an inappropriate statement in the light of many challenges humanity faces today, including the evolution of resistance (from the antimicrobial drug resistance to the resistance to pesticides). Think about other examples where the human future depends on the outcomes of natural selection.

Look back at Figure 2.14d, which shows the two kinds of threespine sticklebacks that live in Paxon Lake. There used to be a similar limnetic/benthic pair in Enos Lake (see Hendry et al. 2009). However, recent studies have revealed that the two forms in Enos Lake have recently merged into a single highly variable population. How does this bear on the claim that the two forms in Paxton Lake are different species? How does it bear on the claim that varying degrees of divergence among stickleback populations provide evidence for speciation?

This study shows that lake and creek fish in the Robert's lake and creek still have the ability to mate, but in the Paxton Lake, fish had evolved reproductive isolation mechanisms between the Benthic and Limnetic populations. Even if they mate and produce hybrids, their offspring has lower viability. In this study, we could see different stages of speciation, based on their genetic differentiation and degree of reproductive isolation. In the case of the Enos Lake, there is no evidence that speciation process went far enough to produce the irreversible reproductive isolation. Thus, we could not apply the biological definition of species. Lake Paxton, however, might not be harboring two different species of stickleback.

Describe three major objections to Darwin's theory in the 19th century that were eventually resolved by dis- coveries by other scientists in the 20th century. What does this tell us about the utility of a theory that cannot yet answer all questions but that appears to be better than all alternative theories?

Three major objections to Darwin's theory in the 19th century were: there is not enough variability for evolution to continue for very long; new traits would disappear by "blending" with other traits; and, the earth's temperature implies that the earth is too young for evolution to have occurred. These were resolved by the discoveries, respectively, of mutation, genes, and radioactivity. The message is that a theory should not be discarded if it cannot answer all questions, especially if it is clearly better than all alternative theories ("better" meaning that it agrees with more data, makes more successful predictions, and has fewer unanswered questions). The unanswered questions should instead be regarded as topics deserving intensive research.

Section 2.4 presented two definitions of homology: the classical definition articulated by Richard Owen and the modern definition favored by many contemporary bi- ologists. Look at the vestigial organs shown in Figure 2.7. Is the tiny wing of a brown kiwi homologous to the wing of an eagle? Are the spurs of a rubber boa homolo- gous to the hindlimbs of a kangaroo? By which defini- tion of homology?

Under the modern definition of homology, a kiwi's wing is homologous to an eagle's wing, and the rubber boa's spurs are homologous to a kangaroo's hind legs. Owen's classical definition is only applicable if the organs are subjectively judged to be "the same organ." Owen would likely have agreed that a kiwi's wing and eagle's wing are the same, but he might not have perceived the rubber boa's spurs as being essentially the "same organ" as a quadruped's hind legs.

Volvox (Figure 8.22a) are abundant and active in lakes during the spring and summer. During winter they are inactive, existing in a resting state. During most of the spring and summer, Volvox reproduce asexually; but at times they switch and reproduce sexually instead. When would you predict that Volvox would be sexual: spring, early summer, or late summer? Explain your reasonin

Volvox will probably reproduce sexually when the environment is changing or unpredictable. In different lakes, this may occur at different times, but in general the most unpredictable change will probably be the long gap between the last generation of the summer and the first generation of the next spring. So, we can predict that Volvox will reproduce sexually in late summer, in the last generation of the year. What do Volvox actually do? Data are sparse, but it is known that most species of Volvox spend the winter as dormant zygotes, so to produce these zygotes they must have reproduced sexually during the last generation of the year. It is not clear, however, just exactly when this "last generation" occurs, or whether they may also reproduce sexually at other times.

Most animal populations have a 50:50 ratio of males to females. This does not have to be so; it is theo- retically possible for parents to produce predomi- nantly male offspring or predominantly female off- spring. Imagine a population with a male-biased sex ratio, say, 70% males and 30% females. Which sex will have an easier time finding a mate? As a result, which sex will probably have higher average fit- ness? Which parents will have higher fitness—those that produce mostly males or those that produce mostly females? Now imagine the same population with a female-biased sex ratio, and answer the same questions. What sort of selection is probably main- taining the 50:50 sex ratio seen in most popula- tions?

When females are rarer, females will be able to find mates more easily than will males and females will have a selective advantage. Parents that produce mostly females will have more grand-offspring, compared to parents that produce mostly males. When males are rare, males will find mates more easily, will have a selective advantage, and their parents will produce more grand-offspring. This is an example of frequency-dependent selection, and is thought to maintain the 50:50 sex ratio seen in most species.

Why is it seldom possible to exhaustively check all pos- sible trees for a suite of taxa? What are some shortcuts?

With all the molecular data evolutionary biologists have in a phylogenetic study, there would be an enormous number of possible variants of evolutionary trees that we simply cannot evaluate. Instead we use computational shortcuts, such as bootstrapping phylogeny estimates or Bayesian phylogeny inference. These and other methods in phylogeny inference are the focus of many research groups today.

Would it be possible for male C. elegans to persist if the proportion of eggs they collectively fertilize is less than their own frequency in the population? How?

Yes, but it requires a strong enough selection advantage for outcrossed progeny (offspring of males) relative to the fitness of progeny produced by selfing (no males involved). This puts specific requirements on the value of w, the relative fitness of outcrossed progeny. According to the equilibrium conditions for the model detailed on page 317, males will remain at a stable (non-changing) equilibrium frequency whenever a w > 2. When the proportion of eggs that males collectively fertilize is less than their own frequency in the population (as this question states), this means that a < 1.0 (a is the fertilization success of males). If we rearrange the equilibrium condition, we can get w > 2/ a . Therefore, in order for males to persist when a is less than 1.0, their relative fitness w must be greater than 2/ a , whatever the value of a is. We know that in all cases for this question, a is less than 1.0, so w must be at least greater than 2 in all cases. However, depending on the specific value of a , w could need to be much greater than 2 in order for males to persist.

We noted on the first page of the chapter that humans vary considerably in height. State a hypothesis about whether this reflects genetic variation, environmental variation, or genotype-by-environment interaction (any hypothesis is okay). What kinds of evidence might settle the question? Are there experiments that, at least in prin- ciple, would decide the matter? Would it be easier to do them with another species, such as mice?

You can propose any of the above hypotheses and make predictions. For example, if height is solely determined by the environment, you would expect that same genotypes show different results in different environments. On the other hand, if human height is purely result of genetic variation, you would expect same height for the same genotype in different environments. It would be very difficult to test this in humans, but you could use identical twin studies. Mice would be a better experimental model system to compare the phenotypic variation in body size, for example. However, when it comes to human height, we are looking at the quantitative trait (polygenic and highly impacted by the environment).

Remote oceanic islands are famous for their en- demic species—unique forms that occur nowhere else (see Quammen 1996 for a gripping and highly readable account). Consider the roles of migration and genetic drift in the establishment of new species on remote islands. a. How do plant and animal species become es- tablished on remote islands? Do you think is- land endemics are more likely to evolve in some groups of plants and animals than others? b. Consider a new population that has just arrived at a remote island. Is the population likely to be large or small? Will founder effects, genetic drift, and additional waves of migration from the mainland play a relatively large or a small role in the evolution of the new island population (compared to a similar population on an island closer to the mainland)? Do your answers help explain why unusual endemic species are more common on remote islands than on islands close to the mainland?

a. Plant and animal species arrive on remote islands by air or by sea. Though the process is highly random, the species most likely to colonize remote islands are (1) those that can travel by air (birds, bats, flying insects, plants with windborne seeds) or (2) those are small enough to be carried by floating vegetation and that can also survive several days without freshwater (many small lizards, insects, etc.). Recently a new category of colonizer has emerged: (3) species that travel with humans. This category includes rats, cats, imported fruits and vegetables, and so on. b. New island populations are usually very small, and are highly affected by founder effects and genetic drift. A new island population that is completely isolated from the mainland population will often diverge quickly from the mainland population, resulting in endemic species. But if the mainland is close, additional waves of migration will probably occur, homogenizing allele frequencies and reducing the effects of genetic drift, and unusual endemic species are less likely to evolve.

Convergent evolution

he process whereby organisms not closely related (not monophyletic), independently evolve similar traits as a result of having to adapt to similar environments or ecological niches.

Hardy-weinberg equation

p2 + 2pq + q2 = 1