Embryology Biology 441 Vertebrate Embryology, Spring 2016 Albert Harris
Review questions for the last part of the course - part one |
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The final exam will be cumulative (in the sense of including questions from all parts of the course).
So please study the previous lists of review questions, in addition to these new ones. You are also responsible for the figures and illustrations posted on the course web pages. The exam may include one or more pictures on which you will need to label something, identify something, or say what is significant. Also VERY important: You should know which germ layer and which subdivision of that layer every tissue or organ develops from (see the review questions for the third exam for the list. For example, olfactory placodes develop from somatic ectoderm; just saying "ectoderm" is not sufficient. -------------------------------------------------- All of our body's cells have a higher?/lower? concentration of potassium ions in their cytoplasm as compared with the concentration of this ion in the surrounding fluid. This difference causes what?
The plasma membrane is normally more/less permeable to which of those two ions? When do oocytes become more permeable to sodium and calcium ions?
What function(s) are accomplished by those increases in ion permeabilities?
Injection of high concentrations of what ion is used for capital punishment in this state?
By what means does this ion kill? Suppose that cancer cells have abnormal ion concentrations in their cytoplasm. How could this be used as the basis of diagnosis? As a basis for treatment? Which kinds of differentiated cells have "resting potentials"? What are the similarities between the fast block to polyspermy and the propagation of nerve impulses? Please include secretion of synaptic vesicles and part of the slow block to polyspermy? Suggest how blocks to polyspermy could be used to prevent pregnancy.
This voltage difference is caused by (Which ions? Potassium? Sodium?)
being more than ten times more concentrated in the cytoplasm as compared with outside cells. Why is a positive voltage outside cells produced by positive ions of a certain element?
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What would happen if an oocyte suddenly became more permeable to sodium ions than to potassium ions? Does that ever actually happen?
Why are such propagated changes in cytoplasmic voltage a better way to produce a change in cell behavior than simple diffusion of hormones or hormone-like molecules Compare the mechanisms of sex determination in flies versus mammals, and as with turtles; and as compared with ants, bees and wasps. Mammals have a special gene on their y chromosomes that causes development of male characteristics: Do flies have an equivalent gene? (on either their x or y chromosomes?.
Why do flies become males if they have one X and one Y chromosome per cell? Why do flies become females if they have two Xs and no Y chromosomes per cell? Why would a human develop as a male if they had two Xs and one Y chromosome in every one of their cells? Why would a fly develop as a (slightly abnormal) female if each cell had two Xs and one Y chromosome?
People who have either type A or type AB blood would quickly die if any of their lymphocytes secreted antibodies whose binding sites have the right shape to fit and bind to the type A "blood group substance". In contrast, people with either type B blood or type O blood do have lymphocytes that secrete anti-A antibodies.
Is it true that immune self-tolerance (not making antibodies that bind to any of your own molecules) is caused by lymphocytes being able to distinguish between self and non-self molecules.
Actually, lymphocytes whose binding sites fit molecules present in the embryo are selectively eliminated (probably induced to self-destruct, by apoptosis.)
Does this selective elimination process (whatever it is) sometimes fail to occur? What is the function of the random DNA splicing that is part of the normal development of the differentiation of both B lymphocytes and T lymphocytes? What would be the result if a lymphocyte failed to undergo this random DNA splicing? What would happen if this DNA splicing occurred too late during the differentiation of a lymphocyte? ("Too late" means after the time when self-destruction is stimulated to occur in those lymphocytes whose binding sites fit normal molecules of your body). What could happen if the normal self-destruction mechanism failed to detect certain molecules? What are some possible reasons why this self destruction might fail to occur? What if a "self" molecule were "hidden" in the myelin of the central nervous system, perhaps tightly wrapped by other molecules? Can lymphocyte binding sites have shapes that fit the binding sites of antibodies made by different binding sites? Hint: Yes, they certainly can. Monoclonal antibodies have been made whose binding sites fit the binding sites of other antibodies.
Why are lymphomas the only kind of cancer that can be cured using mono-clonal antibodies that selectively fit only the cancer cells? Why is this method of curing cancer not profitable enough to be used to save people's lives? How could the same basic method (Binding sites that fit binding sites) also be used to cure multiple sclerosis? Why would this method be much more profitable as a cure for autoimmune diseases than it is as a cure for lymphocyte cancers? ===================
Suppose that a a certain kind of cell crawls actively, and can detect differences and changes in the voltage difference between the inside and the outside of their plasma membranes. Describe two alternative
sets of responses that could produce galvanotaxis A more challenging question: Given that concentration of a chemical is a scalar variable, but electric voltage behaves like a vector, please try to invent more combinations of cell behaviors that could produce galvanotaxis, that depend on directionality of vector variables.
MODIFIED 4/29 8:20 pm: Another somewhat difficult question: How can cartilages elongate directionally unless the driving force is at least a vector, and perhaps a tensor variable? Would that mean that osmotic swelling cannot be the driving force for elongation of cartilages? (since osmotic pressure is a scalar variable) Suppose they really were descended from species whose adults were spherical, how would tensions in their surfaces need to vary (or not vary) as functions of direction and location, in order to cause them to become, and to remain, spherical. Would their internal pressure also need to be spherically symmetrical (equally strong in all directions).
When developing embryos become non-spherical (for example, if they elongate and become approximately cylindrical), then what changes
need to occur in what properties, in order to cause this shape changes?
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