Evolutionary Biology Spring 2016 Study Questions
- 1 Lecture 1 - Jan 19th 2016
- 2 Lecture 2 - Jan 21st 2016
- 3 Lecture 3 - Jan 26th 2016
- 4 Lecture 4 - Jan 28th 2016
- 5 Lecture 5 - Feb 2nd 2016
- 6 Lecture 6 - Feb 4th 2016
- 7 Lecture 7 - Feb 9th 2016
- 8 Lecture 8 - Feb 11th 2016
- 9 Lecture 9 - Feb 16th 2016
- 10 Lecture 10 - Feb 18th 2016
- 11 Lecture 11 - Feb 23rd 2016
- 12 Lecture 12 - Feb 25th 2016
- 13 Lecture 13 - Mar 1st 2016
- 14 Lecture 14 - Mar 8th 2016
- 15 Lecture 15 - Mar 10th 2016
- 16 Lecture 16 - Mar 22nd 2016
- 17 Lecture 17 - Mar 24th 2016
- 18 Lecture 18 - Mar 29th 2016
- 19 Lecture 19 - Mar 31st 2016
- 20 Lecture 20 - Apr 5th 2016
- 21 Lecture 21 - Apr 7th 2016
- 22 Lecture 22 - Apr 12th 2016
- 23 Lecture 23 - Apr 14th 2016
- 24 Lecture 24 - Apr 19th 2016
Lecture 1 - Jan 19th 2016
1) What type of adaptation would you expect to see in an organism living in an environment with visual predators?
2) What’s one possible explanation for powered flight appearing only once in invertebrates and at least three times in vertebrates?
3) Why would it be advantageous for an organism to resemble something else; i.e. a caterpillar that looks like bird droppings or an orchid that smells like carrion?
4) What’s convergence? Can you think of an example we saw in lecture?
5) Do similar traits always evolve because they solve the same challenges? For instance, are bright colors always favored because of their role in getting a mate?
6) In what ways can humans be a source of selection to other organisms?
7) What’s the difference between evolutionary change and plasticity?
Lecture 2 - Jan 21st 2016
1) What is the difference between genotype and phenotype?
2) How might an organism’s environment influence its phenotype? Think of the examples you saw in lecture and come up with two more.
3) In class, we focused on figuring out how to tell if a phenotypic difference was caused by an evolutionary change. What if there is no phenotypic difference between two populations you observe in the wild? Could there still have been an evolutionary change? Why or why not?
4) In class, we talked about the work of Peter and Rosemary Grant on Galápagos finches. Why were these finches a good system in which to study evolution? Give three reasons.
5) What do you predict would happen to finch bill size after another generation, if the rains return? Explain your answer.
6) Define adaptation/an adaptive trait. What happens to the frequency of adaptive traits over generations?
7) What conditions must be met for evolution by natural selection to take place?
8) Why do we think that the loss of armor in freshwater sticklebacks is adaptive, even though we don’t know how armor loss helps their survival?
9) What is one way that the stickleback and finch examples are similar? What is one way they are different?
Lecture 3 - Jan 26th 2016
1) A trait in certain individuals within a population increases their fitness by 3%, can this trait be considered an adaptation?
2) Why were researchers able to use corn to examine the effects of natural selection? What factors made this a good study system?
3) A scientist is studying mice in meadows and has been able to document fitness levels of different genotypes over many years. If this scientist transplanted these mice to a woodlands environment would you expect to see the same trends in fitness in this new environment? Why or why not?
4) You are studying a rabbit species in which some individuals have brown fur and some have black fur. After performing some crosses you are able to determine that the allele for black fur is dominant. With this information can you conclude then that having black fur makes the rabbits more fit than if they had brown fur?
5) How were researchers able to conclude that apical dominance in corn was not a new mutation caused by domestication?
6) Is there a limit on how many bases must be changed by a mutation before this new mutation can be considered adaptive?
7) What are the different ways in which selection can vary?
8) Are there ways that natural selection could act upon a population without producing an evolutionary response?
Lecture 4 - Jan 28th 2016
1) Why was it important for researchers to understand the life cycle of HIV?
2) What method was used for the first treatment of HIV?
3) How was the virus able to rebound after treatment with AZT?
4) What were some of the factors that we discussed that allows HIV to quickly evolve drug resistance?
5) What do we need to know about a study system in order to conclude whether or not evolution has occurred?
6) Do changes in alleles need to be directional in order to be considered an evolutionary change or can they fluctuate randomly? Explain your answer.
7) When organisms are in a changing environment, what do we need to know in order to conclude that a phenotypic change is a result of evolution rather than plasticity?
8) Explain how treating HIV-infected individuals with multiple drugs slows down the evolution of drug resistance. What else can we attempt to slow down the evolution of resistance?
Lecture 5 - Feb 2nd 2016
1) Explain the differences between Mendelian and quantitative traits, and give an example for each.
2) Why can’t we perfectly predict phenotype from genotype for quantitative traits?
3) Fur color in mice depends primarily on the genetic composition at five different loci (A-E). Suppose that each locus has two alleles, and that one of the alleles (called A1-E1) makes fur lighter while the other allele (called A2-E2) makes fur darker. As a result, mice that possess 10 '2' alleles are jet black while those that possess 10 '1' alleles are white.
- A. How many different fur color phenotypes are there (ignoring environmental effects)?
- B. How many different genotypes are there?
- C. How many different genotypes produce the phenotype that is one shade lighter than jet black? (Hint: think about how many different places a '1' allele could occur)
4) Explain what is wrong with the following statement: “Heritability indicates the degree to which a trait is genetic. Traits with high heritability are genetically determined, while those with low heritability are environmentally determined.” Give an example (real or hypothetical) in which a trait is genetically determined, but the heritability is low (or zero).
5) Provide the name and meaning for each term of the following equation: R = h2 * S.
6) How is heritability defined? How can heritability be measured?
7) The slope of the regression line describing the relationship between the number of abdominal bristles in offspring and the number of abdominal bristles in parents is 0.63 in a laboratory population of Drosophila melanogaster.
- A. What is the heritability of abdominal bristle number in this population?
- B. Suppose that the mean abdominal bristle number in this strain is 237 and suppose that a population geneticist imposes selection on bristle number so that the mean abdominal bristle number among those allowed to reproduce is 196. What will the mean abdominal bristle number among the offspring be?
8) Why is heritability dependent on the environment in which it's measured?
9) How are natural selection and sexual selection similar? How are they different?
Lecture 6 - Feb 4th 2016
1) What is the key difference between the “good genes” hypothesis and the runaway sexual selection model?
2) What does it mean to say that male ornamentation and female choosiness are genetically correlated?
3) In pipefish, females transfer their eggs to males, who then fertilize, carry, and care for them. Which sex would you predict is the choosy sex? Which sex probably participates in intrasexual selection? Why?
4) Why do males typically have more variability in their reproductive success compared to females?
5) Peacocks with a large number of eyespots on their tails attract more mates than those with few eyespots. Design an experiment to test whether the number of eyespots in a male’s tail is a signal of his genetic quality (aka how would you test the “good genes” hypothesis in this system?).
6) Does natural selection always oppose sexual selection? Explain your answer.
7) What is the relationship between population genetics and Mendelian genetics?
8) In a population of 550 plants, a single gene (DFR) controls flower color. There are 222 homozygous dominant (DFR/DFR) individuals, 150 homozygous recessive individuals (dfr/dfr), and 178 heterozygotes (DFR/dfr). What is the frequency of the dfr allele in this population?
Lecture 7 - Feb 9th 2016
1) A population contains the alleles D and d. The frequency of D is 0.6 and the frequency of d is 0.4. If individuals mate at random within the population what is the chance that an offspring will have the genotype Dd?
2) What happens to genotype frequencies in a population under Hardy-Weinberg equilibrium in subsequent generations? What happens to allele frequencies?
3) You observe the genotype frequencies of a cow population for 2 generations. The allele frequencies and genotype frequencies do not change. Is this population in HWE? Why or why not.
4) Today we discussed several factors that could have caused a difference between the observed genotype frequencies and the frequencies expected under Hardy-Weinberg Equilibrium within sample 2 from our activity. What were some of those factors?
5) If you observe no change in genotype/allele frequencies between two generations can you conclude that nothing is influencing the population?
6) In a population of 100,000 flour beetles there exists a recessive genetic disease that causes antennae to develop in a “Z” shape when in the homozygous condition. You find 10 individuals with Z-shaped antennae. Calculate the genotype and allele frequencies for this population of flour beetles. Assume that the population is in Hardy-Weinberg equilibrium.
7) Explain why there was an increase in the heterozygote genotype frequencies within the older generation sample (sample 2) in Activity 4.
8) How many generations does it take for a population to establish genotype frequencies in HWE (Hardy-Weinberg equilibrium) given all the assumptions are met?
9) Hardy-Weinberg practice: The major histocompatibility complex (MHC) consists of a suite of genes that play an important role in the immune system. While studying a particular MHC locus in a population of deer found in Connecticut, you discover ample genetic variation. There appears to be two common alleles residing at this particular MHC locus. You characterize the genotype of 200 individuals from this population. You discover 40 individuals with genotype AA, 130 individuals with genotype AB, and 30 individuals with genotype BB. (a) What are the genotype frequencies of the sample population of deer?
(b) What are the allele frequencies?
(c) Given the allele frequencies, what are the expected Hardy-Weinberg genotype frequencies?
(d) Is the population in Hardy-Weinberg equilibrium with respect to the AB MHC locus?
10) Hardy-Weinberg practice: Consider the following pair of subpopulations of a tropical butterfly, with genotype frequencies as shown:
Three biologists head to the field to collect this species, and each ends of collecting 500 individuals.
The first biologist gets altitude sickness easily, so he samples only individuals from the lowlands.
(a) What allele frequencies does the first biologist find (assuming he has a random sample of the population)?
(b) What are the expected genotype frequencies assuming Hardy-Weinberg equilibrium?
(c) How do the observed genotype frequencies compare to the expected frequencies?
The second biologist hates the heat, so she drives up the mountain and samples only individuals from the top.
(d) What allele frequencies does the second biologist find?
e) What are the expected genotype frequencies assuming Hardy-Weinberg equilibrium?
(f) How do the observed genotype frequencies compare to the expected frequencies?
The third biologist is a bit more adventurous, and samples individuals continuously as she hikes up the mountain. Assume that she ends up sampling an equal number from the lowland and mountain top populations.
(g) What are the observed genotype frequencies in the sample obtained by the third biologist?
(h) What are the allele frequencies in this sample?
(i) What are the expected genotype frequencies assuming Hardy-Weinberg equilibrium?
(j) Which genotype(s) is overrepresented in the observed sample compared to the expected sample? Which is underrepresented?
(k)What would the third biologist conclude about Hardy-Weinberg equilibrium?
(l) What assumption that we used in deriving the Hardy-Weinberg equilibrium is violated in this case?
Lecture 8 - Feb 11th 2016
1) What are the four assumptions of the Hardy-Weinberg equilibrium?
2) A population contains individuals that display three genotypes: QQ, Qq, and qq. QQ has a frequency of 0.3, Qq has a frequency of 0.45, and qq has a frequency of 0.25. What is the mating frequency between a QQ and Qq mating pair?
3) In a population it has been found that 1 in 10,000 individuals displays albinism, a recessive condition that causes pale skin and white hair. What is the frequency of carriers of the albinism gene within the population?
4) What HWE assumption does natural selection violate?
5) A population of 100 guppies displays three genotypes: AA, AB, and BB. There are 30 AA individuals, 40 AB individuals, and 30 BB individuals.
a.Calculate the genotype frequencies.
b.Calculate the allele frequencies.
c.The probability of survival for the AA genotype is 0.3, for the AB genotype is 0.9, and for the BB genotype is 0.6. Calculate the mean fitness of the population.
d. What is the frequency of each genotype after selection?
6) An allele in a species of flowers controls stamen length. Individuals with TT have long stamens, tt individuals have short stamens, and Tt individuals display an intermediate length. A researcher surveys a population of 500 flowers and finds that 240 individuals have long stamens, 150 have intermediate stamens, and 110 have short stamens.
a. What are the genotype frequencies?
b. What are the allele frequencies?
7) Imagine that the frequency of allele D is 0.7 in a set of zygotes that you sample. All DD and Dd individuals survive to reproduce, but only 60% of dd individuals survive to reproduce.
a. What is the average fitness of the population in this generation?
b. What will be the frequencies of D and d alleles in the zygotes of the next generation (assuming mating is random and drift has no effect)
c. What will the frequencies of the D and d alleles be in the adults of the next generation?
d. What is the average fitness of the population in this next generation?
8) The fur length of a species of mice is controlled by two alleles: L and S. The observed genotype frequencies are 0.75 for LL, 0.1 for LS, and 0.15 for SS.
a. What would the mating frequency be for a LS and LS mating pair? What proportion of their offspring might be LL?
b. What would the mating frequency be for a SS and LL mating pair? What proportion of their offspring might be LS?
9) At birth the frequency of allele B is 0.45. About 80% of BB individuals survive to reproduce while only 50% of Bb and bb individuals survive to reproduce.
a. What are the genotype and allele frequencies of this generation at birth?
b. What is the mean fitness of the population?
c. What are the genotype frequencies of the adults?
d. What genotype frequencies would you expect the next generation to have at birth?
10) What HWE assumption does mutation violate?
Lecture 9 - Feb 16th 2016
1. What does it mean when an allele has “been fixed” or “gone to fixation” in a population?
2. Fill in the following table:
|Type of selection||Maintains or eliminates genetic variation?||Highest fitness genotype(s)||Initial allele frequency important?||Consequences|
3. What are fitness landscapes? Why are they parabolic?
4. Butterflies that are palatable (tasty to insectivores) often develop patterns mimicking poisonous butterflies to avoid predation. Let’s say a population of palatable butterflies develops two kinds of wing patterns, each looking like a different species of poisonous butterfly. Assume that the mating between two butterflies of different wing patterns produces a heterozygote that doesn’t look poisonous to predators. What kind of selection (balancing/directional/disruptive) would act on this population? How do you know?
5. In a population of 1000 plants, there are two alleles for petal spots: P1 (purple spots) and P2 (no spots). 200 plants have the genotype P1P1, 350 are P2P2, and 450 are P1P2. The fitness of each genotype is as follows: w11=0.7, w22=0.9, and w12=1. What is the mean fitness of this population?
6. From Fisher’s Fundamental Theorem, we know that offspring are more fit than their parents if we make one important assumption. What do we assume, and why?
7. Why can’t we say that balancing selection maximizes the number of heterozygote individuals in a population?
8. Why might balancing selection be more prevalent in the short term than the long term? Use a specific example, real or hypothetical, to support your answer.
9. Why does it take longer (more generations) to fix alleles when fitness differences are very small?
10. Why do we say that the outcome of genetic drift (fixation of one allele) is not predictable?
11. We have already talked about genetic differences that are considered neutral. Can you think of an example of a neutral phenotypic difference?
Lecture 10 - Feb 18th 2016
1. Why can’t we assume that all “functionless” traits (e.g. eye genes in cave fish) are neutral?
2. Which is more likely to be neutral: a non-coding region of the genome, or a protein coding gene? Why?
3. Define and distinguish genetic drift and random sampling error.
4. As you increase sampling (for example, flip a coin 200 times versus 10 times), does the expected outcome occur more or less frequently? Do the extreme rare outcomes occur more or less frequently?
5. Can genetic drift and selection occur simultaneously? Explain your answer.
6. Consider two populations of plants, each with the same two alleles for height: T and t. Assume that there are no fitness differences between TT, Tt, and tt genotypes. Population 1 consists of 10 individuals, while Population 2 has 1000. The frequency of the T allele in both populations starts at 0.7.
- A. In which population will the effects of genetic drift be stronger? Why?
- B. Are these populations more likely to fix the T allele or the t allele? Why?
- C. After 10 generations, researchers discover that the t allele has been fixed in Population 1. Is this result surprising? Why or why not?
7. Explain why genetic drift reduces genetic diversity within a population, but increases genetic diversity between populations.
8. A researcher encounters a small island population of birds, which has been fixed for an allele producing white feather color. On the mainland, the white feather allele occurs at a low frequency (0.1) because it increases predation. The island has no mainland predators.
- A. Give one explanation for the fixation of the white allele on the island that involves natural selection.
- B. Give one explanation for the fixation of the white allele on the island that involves genetic drift.
- C. How could the researcher test whether natural selection or genetic drift was a better mechanism for the fixation of the white allele? Hint: Consider how each of these phenomena operates on the whole genome.
9. How are bottlenecks and the founder effect similar? How are they different?
Lecture 11 - Feb 23rd 2016
1. How many migrants does it take to keep populations from diverging? Why is this the same for small and large populations?
2. What type of shape do you expect to see in the distribution of allele frequencies of populations that are largely independent of one another, hump or u-shaped? What about populations that are mostly dependent on one another?
3. What do N and m stand for in the equation 2Nm>1?
4. What is the difference between parapatric and allopatric populations? Which type would experience the higher migration rate?
5. Why do we want to conserve genetic diversity?
6. We run two simulations, both simulations have the same starting frequency for A1 and the same fitness values for each of the genotypes. The only difference is that the first simulation has a population of 500 individuals and the second simulator has a population of 50 individuals. What differences would we expect to see between the two simulations?
7. What Hardy-Weinberg assumption does migration violate?
8. How do you calculate the migration rate?
9. You are studying several populations of mice and you have figured out that there is 1 immigrant every four generations. Do you think this migration rate will keep the population from diverging? What if the migration rate was 1 immigrant every generation?
10. When can migration possibly cause maladpation?
11. Populations of sand lizards (Uma notata) live in large, isolated sand dunes in the southwestern United States. Herpetologists studying these lizards in Imperial County, California found that the frequency of the Fringe-toed allele was 0.88 in an eastern dune population and only 0.12 in a western dune population. Suppose that a brutal windstorm comes along and blows enough sand around to create a corridor in which some of these lizards can boldly migrate from the eastern dune to the western dune. After the storm is over, 279 individuals are collected from the western dune, 37 of which are from the eastern dune in the last generation.
(a) Calculate the migration rate into the western dune.
(b) What would the frequency of the Fringe-toed allele be in the western sand dune after one generation of migration?
(c) Use this example to explain why a population experiencing migration is NOT in Hardy-Weinberg equilibrium.
Lecture 12 - Feb 25th 2016
1. What are the different types of non-random mating?
2. What is the difference between disassortative and assortative mating?
3. What are the effects of assortative mating?
4. Give an example of assortative mating in which mates are NOT chosen by the way they look. What other types of phenotypic characteristics can also be used to choose mates?
5. Assortative mating by size is very common in nature. Can you think of any explanation for why this type of preference arises so frequently?
6. How can you tell the difference between inbreeding and assortative mating?
7. What is the most extreme form of inbreeding?
8. How are the effects of inbreeding similar to assortative mating? How are the effects of the two different?
9. What is an inbreeding depression?
10. Given what you know about the different types of non-random mating and their effects on genotype and allele frequencies, what would you expect to be the result of disassortative mating?
Lecture 13 - Mar 1st 2016
1) What factors may cause populations to diverge? What factors may keep populations similar to one another? Are these factors evolutionary or non-evolutionary?
2) What is the definition of the term speciation? How do we define (biological) species?
3) Be able to explain what a ring species is. Provide arguments for the existence of one and two/many species in this scenario.
4) What are some of the ways two populations can be reproductively isolated from one another, other than geographically?
5) What is the difference between prezygotic and postzygotic barriers?
6) Which aspects of an organism could result in mechanical barriers to reproduction?
7) Explain how prezygotic barriers might function in plants. (Hint: think about pollinators!)
8) Two populations of individuals belonging to different species produce viable hybrids. In general, what would you expect the fitness of the hybrids to be, relative to the parental individuals? What type of reproductive isolation is this?
9) Does reproductive isolation happen quickly in one step or is it a gradual process?
10) How many reproductive barriers have to be present for us to determine that speciation has occurred? Defend your answer.
Lecture 14 - Mar 8th 2016
1. What is the difference between effective population size and census population size?
2. Explain how David Hillis used phylogenetic trees to provide evidence for the case Louisanna v. Richard Schmidt.
3. What phylogenetic relationship would have indicated that Schmidt was innocent? What relationship would have indicated that he was guilty?
4. What is a monophyletic clade?
5. What is a sister group?
6. Why does HIV have such a high mutation rate?
7. What are some sources of genetic variation?
8. Are the trees below representing the same relationship?
9. Explain what is wrong with the following statements:
A. Humans evolved from chimps.
B. Jellyfish are ancestral to fish.
C. Coelacanths are primitive fish.
D. Humans are the most advanced organisms on Earth.
10. Try these phylogenetic tree practice questions in order to get an idea of what you should know.
Lecture 15 - Mar 10th 2016
1. What are some assumptions you need to make when inferring a phylogenetic tree?
2. Explain the principle of parsimony.
3. What assumption does homoplasy violate?
4. What are some processes that can cause homoplasy?
5. What is the difference between pleisomorphy, apomorphy, and synapomorphy?
6. In class we looked at how to infer the phylogenetic tree for several birds with different color patterns. One of the features we examined was presence of a mask (coloration of the face). When did Dr. Yuan say that this character could be considered pleisomorphic? When did he say it could be considered apomorphic?
7. Which of the three types of characters is used to define clades?
8. Explain and give an example of convergent evolution.
9. Explain and give an example of reversal.
10. How is homology different from homoplasy?
11. Try these inferring phylogenies practice problems
Lecture 16 - Mar 22nd 2016
1. Explain the principle of parsimony. How do you know if one tree is more parsimonious than another? Can two or more trees be equally parsimonious?
2. Is the most parsimonious tree the true evolutionary tree? Why or why not?
3. Why do we have to use computer algorithms to find the most parsimonious tree? (Hint: what happens as we add species/taxa?)
4. What is a character? What is a character state? Give a real or hypothetical example.
5. What major assumption do we make when we build phylogenies from DNA or protein sequences? (Think about homology)
6. What is character conflict? Why does it arise? (Think about the whale example from lecture)
7. Why do we see so much convergence in DNA sequences?
8. Compare the following sequences:
|Position 1||Position 2||Position 3||Position 4|
- A. Which positions are parsimony informative? How do you know?
- B. Which positions are NOT parsimony informative? How do you know?
- C. Do you see any instances of character conflict? Explain.
9. What is an outgroup? What does it tell us about evolution?
10. What are retrotransposons? Why are they useful characters for building trees?
Lecture 17 - Mar 24th 2016
1. What are the three domains of life?
2. How did Woese show that Archaea are distinct from other groups?
3. Why is it difficult to root the tree of life?
4. Name two contributions of Frederick Sanger to molecular biology.
5. Define and distinguish mutation and substitution.
6. Fill in the blanks:
- A. The most important evolutionary force operating on deleterious mutations is ______________.
- B. The most important evolutionary force operating on neutral mutations is ______________.
7. What are synonymous and nonsynonymous substitutions? What does this have to do with the genetic code?
8. What does it mean when the dN/dS ratio is greater than 1? Why are evolutionary biologists so interested in this particular outcome?
Lecture 18 - Mar 29th 2016
1. Only a small portion of the human genome contains genes, what makes up the rest of our genome?
2. What are some differences between prokaryotic and eukaryotic genomes?
3. Explain how transposable elements are similar to viruses? How do they differ?
4. What is a pseudogene?
5. Why do bacteria tend not to have transposons?
6. How can new genes form?
7. What are some possible fates for duplicated genes? What is the most common fate?
8. Why is it important to look at multiple genes when attempting to infer the phylogeny/relationships between different organisms?
9. Why are the genomes of some plants so large?
10. Why are small RNAs important?
11. Does genetic drift or natural selection preserve duplicated genes? Explain your answer.
12. Explain how Antartic eelpouts evolved antifreeze proteins.
13. Explain why elephants don’t get cancer.
14. What is the “chicken or the egg” question in regards to transposable elements?
Lecture 19 - Mar 31st 2016
1. What impact did Schrodinger’s book “What is life?” have?
2. What are the minimum requirements of life?
3. What discovery lead Cech to research splicing?
4. What controls splicing?
5. What are the implications of Cech’s discovery?
6. What is the primordia soup hypothesis?
7. What is the Urey-Miller experiment?
8. Why is it hard to tell if DNA or proteins came first?
9. What are ribozymes?
Lecture 20 - Apr 5th 2016
1. Explain why the Urey-Miller experiment may not be a good simulation for the origin of organic molecules/life.
2. How do we know that the amino acids found in the Murchison meteorite are not just Earth contaminants?
3. What is hydrolysis? Why might it be problematic for the origin of life?
4. Using what you know about the properties of lipids, explain how early life forms could have become encased in a membrane.
5. In the context of macroevolution . . .
- A. What are α and Ω?
- B. If α >> Ω, what process is occurring?
- C. If α << Ω, what process is occurring?
6. What factor/s contributed to the rapid diversification of cichlid fishes and honeycreepers?
7. Explain what a “key innovation” is and how it might lead to an adaptive radiation.
8. What is co-evolution, and how might it contribute to radiations? Give an example, real or hypothetical, that illustrates your answer.
Lecture 21 - Apr 7th 2016
1. What is background extinction? How is it used to define mass extinction?
2. Answer the following about the mass extinction at the K-T boundary:
- A. What was the indirect cause of the extinction event?
- B. What was the direct cause of the extinction event?
- C. Give two lines of evidence that support scientists' hypothesis about what caused the non-avian dinosaurs to go extinct.
3. How are humans causing the 6th mass extinction? Give at least three processes.
4. Compare and contrast phyletic gradualism and punctuated equilibrium. Is one more likely to occur in evolution? Defend your answer.
5. What is morphological stasis? Is it an evolutionary dead end, or an important evolutionary strategy? Give an example to support your answer.
6. What are biological provinces? How did they come about? (Think about Wallace's line)
7. What are the two major mechanisms responsible for spatial and temporal patterns of biotic diversity?
8. How did marsupials evolve? Give a comprehensive explanation including the two mechanisms from question 7.
Lecture 22 - Apr 12th 2016
1. What was the Modern Synthesis? Why was it important?
2. What is heterochrony?
3. What is allometric growth?
4. How do heterochrony and allometric growth differ?
5. What has allowed there to be such a diversity in body plans among plants and animals?
6. What are Hox genes? Why are they important?
7. What subject area is covered by the field of evo-devo?
8. What is the difference between paralogs and orthologs?
9. Define homology. Why would it be important to know whether or not two traits are homologous?
10. Why was development overlooked until the 1980s?
Lecture 23 - Apr 14th 2016
1. What is gene expression?
2. How can you test that a gene is responsible for a specific phenotype?
3. How does gene expression change?
4. What is modulization and why is it important?
5. What are the morphological differences between the marine and fresh water sticklebacks? What is one factor that has led to this difference?
6. Explain what researchers found when they examined the mutations that were responsible for the loss of spines across the different populations of sticklebacks.
7. Changes in ________ ___________ is important for morphological change.
8. What is the role of the cis-regulatory element of a gene?
Lecture 24 - Apr 19th 2016
1. Why are mutations in cis-regulatory elements typically less deleterious than mutations in coding regions?
2. Imagine a plant species whose flowers are purple in low-elevation populations. Researchers discover seven isolated high-elevation populations, each with white flowers. They sequence both regulatory and structural candidate genes that could interrupt the pathway producing purple pigments. In each of the seven populations, a mutant version of the regulatory factor PELAN has been fixed.
- A. How would the researchers determine whether this mutation evolved independently in each population?
- B. Is it more likely that the white mutation become fixed via natural selection or genetic drift? Why?
- C. Give an explanation for why the mutation occurred in a regulatory factor instead of a structural gene. (Hint: purple pigments are found in all tissues of higher plants)
3. What kind of natural selection fixes adaptations? What are the two “types” of this selection, and how do they operate?
4. Why do scientists sometimes refer to evolution as “predictable”? What does it mean to maximize phenotypic output while minimizing pleiotropy?
5. How do novel structures evolve? Is any structure truly novel?
6. What is the key difference between Müllerian mimicry and Batesian mimicry?
7. What is co-evolution? How might it fuel rapid evolution? Give three real or hypothetical examples of co-evolution.