Second Exam Review Questions, Biology 2005 Albert HarrisThe second exam in Biology 104 will cover the material on symmetries, on curvatures, stresses, scalars, tensors and all that, and the material in chapters 6, 7, 8 (but just selected parts of 8_ 9, and 10 (but NOT chapter 11 which will be left until later). I hope everyone will read chapter 8, and look at the pictures, and then not worry too much about the details in that chapter, unless they are also covered in lecture notes, all or which are or will be posted on the web. There are some questions below related to symmetry for which you need to look at certain pictures in chapter 8. Questions with one star * in front of them are so difficult, that you should not worry if you can't figure out the answer. Not more than 5 to 15% of any exam will consist of questions with this one-star level of difficulty. But I hope you will be curious about these; and you are welcome to discuss them with other students, including other students in this course, or anyone. But I hope you won't just ask me, unless you can invent some way to ask me indirectly, like suggesting a possible answer, and asking if I agree! Questions with two stars ** in front of them are even more difficult. I don't intend to put them on exams, except maybe for extra credit. And if you can think of some good answers, them please tell or e-mail them to me, and I will be impressed. Who knows, some day you may want me to write a letter of recommendation! Or you may get the Nobel Prize for inventing the answer.
Although our textbook has only occasional things to say about symmetry, and nothing about tensors, I hope that Curie's Principle and symmetry breaking, as well as the relations between mechanical stresses and surface curvatures, will serve as a unifying theme for this section of the course.
Xenopus frogs originally came from below the equator, and they DON'T actually develop reversed asymmetry of their heart when they gastrulate north of the equator! But what would it imply if they DID? What kind(s) of symmetry does an oocyte have before it's fertilized?
-> 4 planes of reflection symmetry; -> an infinite number of planes of reflection symmetry; -> one, and only one, plane of reflection symmetry. -> Conversion of an embryo from having axial symmetry (infinite number of planes of reflection symmetry) to having only one plane of reflection symmetry. -> displacement symmetry -> conversion to having displacement symmetry by only certain distances, from previously having displacement symmetry by any distance. When embryos develop, do they become more symmetrical, or less symmetrical? Compare that with what changes in symmetry happen when you run cellular automaton programs. List some different kinds of mechanisms that you have learned about for making developing embryos LESS symmetrical than they had been previously, but less symmetrical in the same way for each embryo. A central problem of embryonic development is how to become less symmetrical, but not randomly so: can you give some examples of different ways in which this is accomplished? Contrast the symmetry of an unfertilized frog oocyte, or an unfertilized nematode oocyte, in contrast with the symmetries of an unfertilized fly oocyte. What kind of symmetry (usually? always? tell me if you know of any exceptions) exists between the bodies of pairs of conjoined twins? What about the symmetries of the tadpoles shown in the photograph on page 311 of the textbook? And the one shown on page 323 of the textbook? What about the increased symmetry of the irradiated fly embryos shown in figure 9.9 (page 270) of the textbook? What abnormal symmetries were produced in the experiments described in figure 9.15 on page 275 of the textbook? In what sense does the mechanism of fruiting body formation in Dictyostelium have dilation symmetry? Do the stalks and spore masses have radial symmetry? What about the individual spores? (Although that presumably is coincidental). There is a sense in which homeotic mutations in flies cause an increase in displacement symmetry: explain? To the extent that we imagine that flies evolved from animals whose anatomies were more like centipedes, then what symmetry was getting decreased? Compare or contrast this with the changes in symmetries of the locations of gene transcription of the genes that control early embryonic development and pattern formation in flies. A soap bubble has what kind(s) of symmetry? The forces that are counter-balanced against each other in a soap bubble have what kind of symmetry? What about the symmetry, or lack of symmetry, of rubber balloons? Why can the tension in a sheet of rubber have more asymmetry than the tension in a soap film? Suggest a simple embryological mechanism for making eyeballs become spherical, even if they started out with some less symmetrical shape? If the electro-osmotic pressure inside a cartilage is a scalar variable, because concentrations of chemicals are scalar variables, does that mean this pressure can't vary from one location relative to another? (no) Does that mean that the osmotic pressure at each point cannot vary as a function of direction? (hint: yes) What implication does that have for the mechanisms that cause bones to grow longer in length (in the sense of expanding more in the longitudinal direction, as compared with sideways)? There is a dominant gene in humans that somehow causes a failure in this direction elongation. What kinds of mechanisms can you think of that might cause this? (**And why should such a mutant gene be dominant, rather than recessive?) The color pattern of zebra fish have what combination of symmetries? In Turing's mechanism for generating spatial patterns, what symmetry is broken? Could Turing's mechanism produce stripes, rather than spots? Would you be surprised to learn that apoptosis causes the white stripes on Zebra fish? This is claimed! Changes in what variable would result in more or fewer stripes being formed? * What sort of mutation (in an organism using a mechanism like Turing's to break displacement symmetry) might be able to convert an organism from forming longitudinal stripes to forming spots? ** What sort of genetic variation could cause circumferential bands to form, instead of longitudinal stripes? [Imagine a mutant zebra fish with vertical bands, more like Angel Fish!] ** Why do you think the black stripes on angel fish alternate in width? (check them out, sometime) ** King Snakes have genetic variants with 4 patterns: -1)"chain" like hexagons; 2) stripes along their length; 3) belt-like bands around the body; 4) "Salt and pepper" tiny black and white spots. Sometimes a single gene difference can cause one of these patterns instead of another. What mechanisms do this? What about the symmetry of the color pattern of zebras? * The stripes become narrower on zebra's legs; and progressively narrower in proportion to the diameter of the leg: so that is sort of an example of what kind of symmetry? How is curvature defined? Does a bigger circle have more curvature, or what? On the surface of a cylinder, the curvatures in perpendicular directions are what? What about the curvatures of a plane surface? A spherical surface? A saddle-shaped surface? When a soap film is supported around its edges by a bent piece of wire, why are its curvatures like that of the part of a saddle where you sit? * Could you draw the directions of maximum and minimum curvatures on the surface of an egg? *What about on the surfaces of a telephone receiver, or a statue, or a random pebble?
Explain how lymphocytes are the most important exception to the rule about differentiated cells all containing the same combination of genes: explain in what way, and for what purpose, are lymphocytes exceptions.
I hope no one will be offended if we use contraception as another central theme around which to organize and test your understanding of the mechanisms that regulate fertilization of oocytes. Consider the following possibilities: what would the results be, and why; and would it be an effective method of contraception, why or why not, and which ones might be morally objectionable?
2) What if the vitelline membrane were somehow strengthened, so that enzymes couldn't digest it? 3) What if all membrane fusions were somehow prevented from occurring? 4) What if the cortical granules (= vesicles) of oocytes were prevented from releasing their contents? 5) If these cortical granules were caused to be secreted prematurely, before any sperm reached the oocyte? 6) What if calcium ion concentrations inside oocytes were increased artificially, and prematurely? 7) What if those calcium channels were permanently blocked? 8) What if the plasma membrane of oocytes was made completely NON-permeable to potassium ions? 9) Suppose that sperm DNA could be destroyed or permanently inactivated, in some sperm, while leaving these sperm otherwise normal in their abilities to swim, to release enzymes, fuse with oocytes, etc. 10) What if the second meiotic division were prevented from occurring? 11) What if the electrical voltage across the plasma membrane of oocytes were prematurely decreased? 12) What if this voltage were permanently kept large? 13) What if sperm or oocytes were changed so that their plasma membrane could still fuse just as well whether or not this "resting potential" (voltage difference) existed? 14) If a salt solution with a high concentration of potassium were to reach the oocyte before the sperm? 15) What if a drug prevented meiosis? 16) What if a drug blocked the formation of the second polar body, in oocytes? (its nucleus was retained) 17) Can you invent any more potential (no pun) methods for contraception? Perhaps by using either the chemical IP3 (see page 206 & 7) or by preventing the synthesis or binding of IP3?
Is it conceivable that oocytes of some species are always fertilized before the completion of meiosis? What about fertilization before either meiotic division has occurred in the oocyte? What sense does it make that, in sperm formation, meiosis begins and ends before cell differentiation? What sense does it make that differentiating oocytes keep all 4 sets of chromosomes as long as they can? Why is 2 sperm just as bad as no sperm, for producing fertile offspring? What is meant by "polyspermy"? Imagine a genetic mutation that caused sperm having it to swim faster: would such a genetic variant be favored in evolution, or not? What about a gene that increased the probability of successful fertilization by a sperm that has that gene, but also somehow caused the death of any animal that was homozygous for that form of the gene? (i.e. a mutation in a gene that has two effects: 1) makes sperm more successful 2) but kills embryos that have two copies of that gene! Only animals heterozygous for this genetic variant can survive! Hint: examples of this actually occur) Suppose a genetic mutation had the effect of allowing a sperm with that gene to fertilize eggs that had already been fertilized by another sperm: Why would this mutation NOT be favored by evolution? HINT: suppose, on the other hand, that these mutant sperm also had some method for getting rid of the nucleus of the other sperm, that had fertilized the oocyte previously: why could that mutation be favored by evolution, and its frequency on the population increase? Some species have mechanisms for inactivating all but one of the sperm that succeed in fusing into the cytoplasm of an oocyte; what would this accomplish? What sorts of mechanism would it substitute for? A variation is for all but one sperm to be cleaved off, inside their own tiny cells, somewhat like Napoleon being exiled to an island. Can sperm swim in all species of animals? What are some exceptions? Remember that non-disjunction during meiotic divisions can result in embryos that are trisomic for one or more of the chromosomes? What is the effect on embryonic development of trisomy for any chromosome other than the twenty first chromosome (trisomy for either of the sex chromosomes X or Y, is not so serious, although I didn't mention it). What is caused by "trisomy-21"? When do oocytes begin meiosis in mammals, including humans? When does the second meiotic division occur, in human oocytes? In the cells that will become sperm, when do the first and second meiotic divisions occur? If non-disjunction occurred in one of these cells that will become sperm, why would the resulting sperm itself probably be much more abnormal (and unable to participate in fertilization) than an oocyte will be if it (the oocyte) undergoes non-disjunction in one of its meiotic divisions? Discuss why this might explain why the probability of producing mentally retarded children is not in increased so much when the father is older than 35 or 45, or 50, etc. in contrast to what the probability when the mother is older than 35? (Hint: there are at least two aspects to this question; one relating to when meiosis begins and ends, and the other having to do with when sperm and oocytes undergo differentiation relative to the times they complete meiosis. And notice that there is a very dangerous form of cancer that seems to be caused by a normal sperm fertilizing an oocyte that had somehow lost its nucleus. Some species and subspecies of lizards and fish have only females, and instead of fusing with sperm, their oocytes resorb the second polar body; explain why this allows their embryos to be diploid, despite no fertilization?
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