Embryology Biology 441 Spring 2007 Albert Harris and Andrius Masedunskas
Review Questions for Final Exam
Fourth List of Review Questions (for lectures since the third exam)Imagine that you are designing a "genetic screen" to find animals with mutations in (just!) those genes that control eye development in flies, approximately how would you do this? Besides looking at all the flies' eyes, can you imagine some way to select out mutants based on the flies' own vision? Suppose that most mutations of a certain gene produce no detectable effect, and that the only mutations that produce any effect cause death of the mutant animal (even animals that are heterozygous for the mutation!): explain why a genetic screen is going to be blind to this gene, and not detect its existence.
How do new genes get discovered, usually. When genes are named, are they named after the function of the gene, or something very different. If a gene were called "Marie Antoinette", or "Charles-the-First", then the normal version of the gene would probably be necessary for the development of what part of the body? What if a gene were named "scarecrow"? What organ would fail to develop normally in animals in which this gene is mutated?
What are at least three important advantages of using flies for genetic (or any other) research? What are at least four fundamental differences between the embryonic development of flies, in contrast to the embryonic development of humans, birds, frogs, sea urchins, etc.? What is a syncytium? What is a specific example of a syncytial tissue, besides human skeletal muscles? Where are imaginal discs located, in what kinds of animals, and what do they eventually develop into? Does it ever happen that a certain mutation causes a certain imaginal disk to develop into a different organ than it would have developed into in an animal lacking that mutation? What are such mutations called? Name at least one specific example of such a mutation, and describe its effect? Genes that can be mutated to produce this class of effect on anatomical structures probably code for proteins that serve what function (based on past research)?
Embryologists use the method called "in situ hybridization" to map the locations of what chemicals, and to map where what process is localized (hint: transcription of messenger RNA of certain genes). What is a hox-box? What is a homeodomain? If a gene contains a hox-box, what function does it serve in normal development? What part of this gene's protein binds to certain locations on DNA? For what purpose? What are the five main families of genes that have been discovered in studies of fly development? Sketch the approximate spatial distributions where genes of each family are transcribed before and during fly development. The transcription of the genes in each of these families of genes is controlled by what?
What are hox genes? Are they found in any animals besides flies and other insects? Are they found in humans and other mammals? Is there any similarity in linkage maps of the locations of hox genes on chromosomes, relative to the locations in the developing embryo where each given hox gene is transcribed? Is it usual for all or most of the genes needed for, say, liver development, to be found next to each other on the same chromosome?
Thought question: Imagine if genes whose base sequences are very similar to "pair-rule" genes also occurred in vertebrates, and if mutations in these genes caused abnormalities in somite formation: What sense would this make? If this occurred, and you had the materials to do in situ mapping of the the m-RNAs coded for by these genes, then what pattern would you look for? What different result might you expect? And what would these results tell you about the mechanism of formation of somites?
Sex determination in flies is somewhat similar to sex determination in mammals, but different in more fundamental ways: What are some similarities? What are some differences? What is the SRY gene? What chromosome is it located on? Is there any equivalent gene in mice? Is there any equivalent gene in flies? Is this gene ever located on the X chromosome? (hint: yes) What happens when it is? What are autosomes? Do sperm contain autosomes? How many autosomes does each sperm cell contain, in humans? How many Y chromosomes does each sperm cell contain, on the average? (for example, 100 sperm cells would contain a total of about how many Y chromosomes?). Suppose that a gene on a Y chromosome were mutated in such a way that sperm containing this mutation would swim faster, or otherwise have unusually good success fertilizing oocytes: what would the longer term effect be? Imagine if a gene on an autosome could be mutated in a way that tended to cause autosomes containing it to remain in the oocyte during meiosis, and not pass into either of the polar bodies: what long term effect would this have on the frequency of this mutation in the population? Would this effect still occur even if this autosomal mutation were lethal when homozygous? (hint: yes) Does this count as natural selection? How can the sex ratio of humans (or flies) be anything but 50% : 50% ? In fact, IS the sex ratio slightly different? If you could separate X containing sperm from Y containing sperm, for example by centrifugation or electrophoresis, why would this decrease the number of abortions done in the world? How does the sex determination mechanism of birds differ from that in mammals? What is different about the mechanism of sex determination in turtles and alligators? Are there any kinds of vertebrates in which individuals start out as being one sex, but then spontaneously change to become the other sex? A fly that has one X chromosome per cell, and no Y chromosome, will develop into what? Why? In contrast, what would be the sex of a human or other mammal that had one X chromosome, and no Y chromosomes in its cells? What is a gynandromorph? Why do they develop among insects, but not in vertebrates? What is the effect of androgen insensitivity syndrome? If a somatic mutation occurred in a certain gene during a mammal's development, how could that produce something like a gynandromorph? If two mouse blastocyts were fused early in development, one of which would have developed into a male, and the other of which would have developed into a female, then what would probably determine the sex of the chimeric mouse? How would the expected result differ from what would occur if it were possible to do an equivalent experiment with fly embryos? What are 3 examples of hymenoptera, and what is their mechanism of sex determination? Why does this method of sex determination tend to favor the evolution of genetically-caused instincts for altruistic behavior (risking one's life to save another individual)?
Besides the development of unfertilized eggs, what is another kind of asexual development? What kinds of animals can sometimes bud off new individuals from their somatic tissue? Does this occur in lower, primitive phyla? Are there any members of our phyla that reproduce partly in this way? What is meant by "sorting out" of dissociated cells? Who discovered this phenomenon? In what kinds of animals? And later in what other kind of animals? What kinds of animals did Johannes Holtfreter use to study this phenomenon? Did he use developing embryos, or adult animals for this purpose? What hypothesis about cell sorting out was proven true by Moscona and by Trinkaus? How did they prove this? What was the alternative hypothesis (believed by H. V. Wilson)? What are N-CAM and "cadherins"? How did they get discovered? What are the key ideas on which Steinberg based his "Differential Adhesion Hypothesis"? What was his key supporting evidence?
What are at least four different examples of metamorphosis (in different kinds of animals)? What are at least five different changes that occur during the metamophosis of tadpoles into frogs? Compare these to the changes that occur in the metamorphosis of flies and butterfles. How are imaginal discs related to metamorphosis in insects? What is Evo-Devo? Who was Ernst Haeckel? What is meant by the hoary old slogan "Ontogeny...etc." To what extent is it somewhat true? Do embryos tend to resemble the adult form of their ancestors, or resemble the embryonic forms of their ancestors? How can this be explained in terms of the low probability of mutations producing good effect, combined with multiple independent effects tending to be produced by mutations that affect early development?
Explain why "life expectancy" is usually a misleading measure of the rate of aging in human populations (but perhaps less misleading for domesticated animals!)? Hint: How would increased infant mortality change the calculated "life expectancy" in a country? Would the death of more babies really mean that adults would age at a faster rate, much less that the maximum age would decrease? Actually, maximum ages might even be increased by factors that increased infant mortaility! Can you draw graphs
b) Of % dying at each age.
c) Of % dying in the next year, having reached a given age.
For which of these methods of graphing mortality data is it easiest to deduce the "life expectancy"?
For graphing method "b", what part of the curve suggests itself as a measure of when aging occurs?
If you hypothesized that aging and infant mortality were both caused by the same hardships and wear and tear of ordinary life, then how could you confirm this (if true!) by using graphs of the "b" kind?
What aspects of graphs of the "c" type seem to suggest that aging may result from damage that itself increases the frequency of more damage occurring, eventually causing death?
What did Gompertz discover? Why might you expect that sponges and Hydra might not age? What if some kind of animal reproduced ONLY by asexual budding: would they age? How are telomeres thought to be related to aging, or at least to the senescence of tissue culture cells?
Graph the resistance of animals to stress (cold, heat, blood loss, and building renovations) as a function of age. Suggest how differences in the shape and slope of this graph ought to change the graphs of death rates as a function of age (for example, when graphed by any or all of the 3 methods above).
If differences in telomere renewal were the true cause of aging, then how could this be revealed by some or all of these different methods of graphing death rates, or graphing death caused by different amounts of stress on animals of different ages?
[These last two questions are quite difficult, and require difficult reasoning processes. So, if the answers are not immediately obvious to you, then don't panic! But I might really ask some such question on the exam; so think hard about these questions, and don't hesitate to ask other students what they think the answers might be. However, if you ask me, I will get very "Socratic" and vague.]
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