Embryology Biology 441 Vertebrate Embryology, Spring 2016 Albert Harris
Review questions for the last part of the course - part three
62) What is Labyrinthula? What is its economic importance? What is very strange about its cytoplasm and plasma membranes?
63) What are the stages in the Dictyostelium life cycle?
64) Describe the process by which particles are transported on the surfaces of tissue cells in culture.
65) How does the same process operate in cells growing on a flexible substratum? What relevance does this have to formation of structures within the body?
66) What is believed to exert the forces in the crawling locomotion of tissue cells?
67) What is contact inhibition of cell locomotion? Who discovered it?
68) Which of these statements is true?
b) Blockage is caused by thickening of artery walls.
69) What materials cause atherosclerosis? Where are they located? Are they inside the lumen? Are they surrounded by the endothelium? Or are they outside the endothelium (in the place where healthy arteries have only smooth muscle cells)?
70) What is an atheroma? Where is it located? What does it cause?
71) What are endothelial cells? Are they endodermal, despite what the name seems to suggest? Hint: no.
72) What is neoteny? What is an example of neoteny? There are no neotenic echinoderms, but what would an adult neotenic echinoderm look like if such a thing existed?
73) What are at least seven different changes that occur in metamorphosis of tadpoles? Do they all occur at once, or in a sequence?
74) How is this sequence related to the concentration of thyroxine? Is there a way to make all the changes happen at once?
*75) Is there a way to make them happen in the opposite time sequence to the normal order? (If you think of one, let me know).
76) If you grafted other organs to the tail of a tadpole, would these tissues also be destroyed during metamorphosis? Why or why not?
77) What are newts? What is different about their metamorphosis?
78) What is the relationship between molting and metamorphosis in insects and other arthropods? Can you have molting without metamorphosis? Can you have metamorphosis without molting? Explain why or why not.
79) How can you make gigantic caterpillars (assuming you would want to)?
80) Are there veterinary uses of this knowledge about juvenile hormone? Explain.
81) Suppose you had a chemical analog of ecdysone that blocked the receptors for normal ecdysone. What would its effect be, and what uses could it have?
82) What are the distinctions between carcinomas, sarcomas, lymphomas and leukemia?
83) What are oncogenes? Give at least three examples, including the names of the genes and the type of protein they encode.
84) People have sometimes said: "If we could just get rid of all the oncogenes, then cancer could not occur." Please explain briefly why this is a misguided idea.
85) Why is blocking the activity of an oncogene not a cure for cancer?
86) How are checkpoint controls in the cell cycle related to cancer and to cancer treatments?
87) How might cancer be treated by a chemical analog of glucose that is poisonous?
88) Suggest a relationship between drugs that inhibit mitosis or DNA synthesis, and how they are related to killing faster growing cancer cells.
89) What does metastasis have to do with the importance of detecting cancers as early as possible?
90) What morphological differences do cancer cells have? What is known about those differences in relation to the lack of growth control of cancer cells? Hint: is anything known?
91) Imagine inventing a new cure for cancer. What property would you target, and would you need to combine with what other properties? If in doubt, explain your reasoning.
92) Is apoptosis likely to be important in treating cancer? Why or why not?
93) Give an example of a cancer treatment currently in use, what drugs are used, and how they are supposed to be related to treating the cancer.
94) What is the biological effect of cyclophosphamide? Why might cyclophosphamide be expected to produce effects similar to aging?
95) What is the biological effect of vinblastine?
96) Explain why it could be useful to have a drug that selectively stops DNA synthesis and mitosis in normal cells but not cancer cells.
97) Could such drugs also be useful if they affected cancer cells but not normal cells? If in doubt, explain your reasoning.
98) Suppose a mutation caused DNA repair to be less effective. Would you expect that to influence life span? Explain your reasoning.
99) If you had a method for measuring DNA repair in different kinds of animals, how would you expect the results to be correlated with their life span?
100) What is the approximate life span of each of the following animals: human, cow, mouse, rat, opossum, elephant?
101) What are some species of animals that age much more slowly than the ones in the list above?
102) After what age does the death rate of humans increase by a constant ratio every year?
103) About how much does the death rate increase every eight years?
104) What makes Drosophila a good research organism? What is meant by a genetic screen?
105) What is peculiar about the early cleavage divisions of fly and (most!) other arthropod embryos, up until about the 6,000 cell stage (in contrast to any vertebrate embryos)?
106) What are imaginal disks? How are they involved in insect development, and in the metamorphosis of larvae into flies, and caterpillars into butterflies?
107) If the effect of a mutation is to cause a fly to develop an extra pair of legs where its antennae should be, what kind of mutation is this called? What went wrong?
108) Do any other kinds of animals have genes with base sequences similar to the genes that can produce this kind of abnormality when mutated?
109) What are the three classes of genes involved in fruit fly development? Give an example of a gene or type of gene in each class.
110) What is meant by "maternal effect" in insect development?
111) What was the name of the 19th century biologist who invented the once popular phrase "ontogeny recapitulates phylogeny"? Hint: Haeckel
*112) When animals were evolving fundamentally different eye structures, did they also evolve different transcription factor proteins to control eye development? Yes or no? Why or why not?
113) Would you expect genes that affect earlier events in embryonic development to evolve more slowly than those that affect later stages, or the reverse? How is the answer to this question related to the idea that ontogeny recapitulates phylogeny?
114) In what sense is the geometric pattern of broccoli the result of a homeotic mutation? The mutation in question causes each petal of the plant's flowers to try to develop into an entire what?
115) Fractals are an example of what kind of symmetry? What are some examples of vertebrate embryonic structures that develop as fractals? What does this have to do with broccoli?
116) Causes of embryological phenomena can be divided into Genetic, and what other three categories?
117) Does embryology of some animals depend on some but not all of these, or do all animals have all of them?
118) If we had not evolved from fish, what would be different about our embryonic development?
119) If we had not evolved from sea squirts, what would be different about our embryonic development? hint: remember that developing sea squirts have notochords and no other invertebrates do
120) Why was it surprising that the Pax-6 gene controls location of development of eyes in insects and also in vertebrates?
121) What does this suggest to you? Does it suggest that evolutionary changes in embryological processes occur faster than the amino acid sequence of signaling molecules, or the reverse, or what?
122) What would be some medical uses of a method that could cause cells of one differentiated cell type to convert to cells of a different cell type?
* 123) Invent a mechanism that might explain the near-irreversibility of cytodifferentiation of animal cells.
Non-mandatory topics for possible discussion on the final exam: You could argue pro or con about any of the following questions, statements and conclusions.
Because mutations are random, they are much less likely to produce improvement than harm, or to be lethal. What factors would you expect to influence the probability of any given genetic change being favored in evolution?
Please consider, for example, mutations that alter the structures of eyes, as compared with mutations in genes that code for transcription factors that control where eye tissues will differentiate. Which mutations would have the greater probability of being lethal?
How does the probability of mutations being lethal or otherwise harmful influence the rate of evolutionary change in any given gene?
Conversely, what if mutations in one gene are twice as likely to increase reproductive success, compared with mutations in another gene? Do you see that evolutionary changes in the former gene will progress more rapidly?
Next, ask yourself whether probability of mutations being harmful ought to be related to the stage of development when a given gene acts. Would genes that act earlier evolve faster or slower? Or should genes that act later in embryonic development therefore have a slightly smaller frequency of lethal mutations?
I would suggest that the answers to these questions are important in relation to "Evo-Devo", and also to Haeckel's concept of recapitulation. The smaller the frequency of mutations of a given gene having favorable effects, the slower that gene will evolve. Genes that act earlier in development tend to change more slowly during evolution; genes that control later events evolve faster.
Do you agree about these tendencies? i.e. that "earlier-acting" genes evolve slower? And that speeds of evolution result from relative probabilities of having lethal versus beneficial mutations?
Lastly, on what basis can we expect "earlier-acting" genes to have the smaller frequency of non-lethal mutations. Perhaps because "earlier-acting" mutations tend to have more side effects. Imagine that a certain mutation has two effects, and that each of these effects has a large and independent probability of being lethal? The more side effects a mutation has, the greater the chance that one or the other effect will be lethal: Therefore, the more different effects are produced by mutations in a given gene, the slower favorable mutations can be accumulated in that gene, which means its evolution will be more conservative. What factors influence the number of different side effects will be produced by mutations in each given gene?
Please consider whether genes which produce their effects earlier in development will therefore be the ones whose mutations produce the most side effects. Would those genes be more or less conservative (i.e. slower of faster) in respect to evolutionary change?
Does this explain Haeckel's "Law" about ontogeny recapitulating phylogeny? Does it explain any other trends in relations between embryonic development and evolutionary ancestry?
As you may know, one of the arguments used to support belief in "Intelligent Design" is that certain structures are so perfect that any mutation affecting them will be lethal. Argue pro or con.
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