Embryology   Biology 441   Spring 2010   Albert Harris   Last set of review questions for Embryology 2010, conclusion     What sometimes happens if you cut off the end of a limb bud (either of a developing chicken embryo limb, or a regenerating newt leg) and graft the tip back into place with its anterior-posterior axis reversed? How is this explained in terms of Bryants' theory of polar coordinates? Can you interpret what happens in terms of cells somehow detecting that some of them are next to neighboring cells that they should not normally be next to, and repairing that abnormality by the equivalent of regenerating whatever parts of the leg would normally be between the two groups of cells that have been put next to each other (but that are not supposed to be next to each other). What different experimental result did John Saunders discover when he cut off the outer end of a chicken embryo limb bud, and grafted it to the side of another limb bud, with the anterior-posterior axis of the graft oriented backwards (in the reverse direction as the limb bud that it was grafted onto). * Extra credit if you can invent and explain how Saunders's result in that experiment can be explained in terms of the normal mechanisms of limb development. Argue pro or con whether the polar coordinates theory is really about development being a series of many close-range, nearest-neighbor cell-cell interactions, even though it was expressed in terms of "positional information". Argue pro or con whether regeneration of legs in newts should be thought of as an example of sorting out of differentiated cells, based on the observation that the skeleton of the new leg is made entirely of descendants of cells that had been chondrocytes in the stump of the amputation, and that the muscles of the regenerated leg are descended from muscle cells in the stump. Why do ducks have webbed feet? (In terms of embryological mechanisms.) In chickens' feet, why aren't they webbed? What are at least three other examples of apoptosis? Draw and describe differences between cancer cells and normal cells, based on the time lapse movies of tissue culture cells that you were showed in class. In what ways can malignant cells be distinguished from non-cancerous cells in histological slides? Suggest how these differences in fixed and stained cells are related to the various differences in cell contractility and movement that you were told about in lectures, and in the videos you were shown. Suggest how differences in invasiveness might be explained by over-activity of two or more specific oncogenes. Draw and describe the geometric patterns of connection of nerve fibers that form the optic nerve. What is a neural projection? What are at least two examples of neural projections? Describe the shape and movements of a nerve growth cone. Do nerve fibers extend from the brain to the eye, or vice versa. Do sensory and motor nerve growth cones crawl from the spinal cord to the periphery of the body, or vice versa? If the eye were cut out of early embryos and implanted back into the head upside down and reversed in the anterior posterior axis, how would this change the connections between the neural retina and the optic tectum? Hint: Would the effect be different, depending on how early in development you made this rotation? What happens if two retinas are forced to innervate the same tectum? What effect do ephrin proteins have on the crawling locomotion of optic nerve fibers? Does this effect vary in proportion to the number of ephrin recetors in the plasma membranes of each individual optic nerve growth cone? Based on the theory that matched gradients of ephrins and ephrin receptors cause the projection of the optic nerve, what ought to happen if the growth cones of the optic nerve were somehow guided so that they arrived at the neural projection on the opposite side of the tectum from where they normally arrive? (Please give this one some thought.) *Could over-expression or under-expression of ephrin receptor protein cause cells to crawl more invasively than normal? If two of the chromosomes in one of your cells happen to break, and then rejoin in the wrong combination, how could that cause cancer? Would it depend on which differentiated cell type the break occurred in? For example, if chromosomes break and rejoin so that the bcl-2 gene is adjacent to the promoter region of the gene for antibodies, why does that only cause lymphomas? Why doesn't that cause skin carcinomas, or adenomas of the large intestine? What if some different oncogene were translocated to a position on a chromosome that codes for insulin, for example, or for hemoglobin, or for some other "luxury" gene transcribed at a high rate only in some specific differentiated cell type ? What are the normal functions of the genes that, when mutated in an unlucky way, become the oncogenes named ras, src, sis, erb2 and myc? *What sense does it make that injecting teratoma cells into the coelom (of an animal of the same species as the teratoma came from), each teratoma cell will divide and then form a hollow ball, with a bunch of cells at one side? (Hint: you can fuse these balls of cells with blastocyst stage embryos, and get them to develop into chimeric animals, with half their tissues genetically matching the cells of the teratoma!)

 

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