Review questions for the last part of the course

1) What are cotyledons? Draw the shape and locations of the two cotyledons of a peanut.

2) Is a plant seed equivalent to a newly laid egg; or is it more like a neurula stage that has gone into hibernation?

3) What is the difference between cell walls and cell membranes?

4) List major similarities and differences between development of higher plants and vertebrate animals.

*5) How is development of colonial sea squirts and corals somewhat more like plants, at least superficially?

6) What are meristems? What are several kinds of meristems, located in different parts of plants?

7) What is a cambium? What function does a cambium serve?

8) What geometric shape is a cambium?

9) What would a plant be unable to do if it didn't have any cambia? (=plural of cambium) (Latin second declension, neuter)

10)In plants, mitotic divisions are located where?
In meristems and cambium

11) Are these the same places that growth (in the sense of increases in volume) is concentrated?

12) What function does osmotic pressure serve in plant growth?
expands cells, often preferentially in certain directions or locations

13) Compare the "growth" (enlargement and shaping) of plant stems and leaves with that of cartilages.

14) What is an example of a plant hormone that can cause physical weakening of cell walls? How is plant cell growth related to weakening of cellulose cell walls?
Hint: auxin

15) By what systematic series of experimental procedures was indole acetic acid eventually discovered to be (the, until then hypothetical substance) "auxin"?

16) Besides stimulating elongation of shoots, what other effects has auxin also been discovered to stimulate?
phototaxis, geotaxis, root formation, including redifferentiation of stem cells into root cells

17) Which of these effects was used in the actual bioassays by which indole acetic acid was discovered to be auxin?

18) What are anti-auxin herbicides, like 2,4-D?

How were these (multi-billion dollar per year) herbicide chemicals discovered?
(Or would you argue, either pro or con, that they were invented?)

*19) Based on auxin's different effects on plant cell enlargement and differentiation, would you expect Lewis Wolpert to regard auxin as a morphogen?


20) All of our body's cells have a higher concentration of potassium ions in their cytoplasm as compared with the concentration of this ion in the surrounding fluid. This difference causes what?

21) The plasma membrane is normally more/less permeable to which of those two ions?
If a cell became impermeable to potassium ions, what change would this produce?

22) When do oocytes become more permeable to sodium and calcium ions?

23) What function(s) are accomplished by those increases in ion permeabilities?
In nerve axons?
In oocytes?

24) 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?

25) Which kinds of differentiated cells have "resting potentials"?

26) 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?

27) Suggest how blocks to polyspermy could be used to prevent pregnancy.

28) Are nerves and muscles the only differentiated cell types in which the voltage of the cytoplasm is more negative than the voltage of the fluids outside the plasma membrane?

29) 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?
(hint: Potassium) being more concentrated inside of cells? ) (Hint:leakage)

30) What would happen if an oocyte suddenly became more permeable to sodium ions than to potassium ions? Does that ever actually happen?
(Hint: yes; and this change in permeability serves what very important function?

31) 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
(hint: depolarization propagates much faster than simple diffusion).

32) 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
(Hint: galvanotaxis is locomotion toward or away from increasing electric fields).
Further hint: remember those two different ways of producing chemotaxis.

What would the net result be if a cell turned randomly every time it detected an increase in the magnitude of an electric fields?

33) 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.

34) 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)
(Hint: why not?)


35) What is metamorphosis?

36) What are at least three different examples of metamorphosis (e.g. Caterpillars change into what? Plutei change into what? Tadpoles change into what?)

37) What are at least seven different changes that occur in metamorphosis of tadpoles? Do they all occur at once, or in a sequence?

38) What is thyroxine? What functions does it serve? (You don't need to know the molecular structure)

39) 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?

40) How is this sequence related to the concentration of thyroxine? Is there a way to make all the changes happen at once?

*41) 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).

42) If you grafted other organs to the tail of a tadpole, would these tissues also be destroyed during metamorphosis? Why or why not?

43) What are newts? What is different about their metamorphosis?

44) What is ecdysone?

45) What is meant by molting, in relation to the growth of insects and other arthropods?

46) What is Juvenile Hormone? (again, what is its function, not its chemical structure)

47) Does Juvenile Hormone participate in the control of molting and metamorphosis of insects? What does it cause? What does it prevent?

48) 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.

49) How can you make gigantic caterpillars (assuming you would want to)?
Hint: the method involves hormones

50) Are there veterinary uses of this knowledge about juvenile hormone? Explain.

51) 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?


52) A common misconception is that people today live much longer than they did a few hundred years ago. Explain why they are wrong.
Hint: What is the meaning of "life expectancy"?

53) What if aging were caused by effects of somatic mutations specifically in the genes that code for DNA repair and replication. What statistical patterns would be / could be predicted in changes in death rates as a function of age?
Hint: would you expect the symptoms of aging to accelerate with time? Explain why or why not.

54) What if aging were caused by defects in telomerase enzyme:
First: Could you predict any observable statistical pattern in death rates as a function of age?
Second: Could you predict which specific genes would first become defective?

55) Suggest several different possible explanations why primordial germ cells don't age.

56) Draw a graph showing the changes in death rates over the human life span. What is meant by "Gompertzian"? 57) Suppose a mutation caused DNA repair to be less effective. Would you expect that to influence life span? Explain your reasoning.

58)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?

59) What is the approximate life span of each of the following animals: human, cow, mouse, rat, opossum, elephant?

60) What are some species of animals that age much more slowly than the ones in the list above?

61) After what age does the death rate of humans increase by a constant ratio every year?

62) About how much does the death rate increase every eight years?

63) Briefly explain something that you learned in this course about the process of aging.

64) Suggest what (if anything) it implies about the mechanism of human aging that death rates increase logarithmically past a certain age (which is about 35).

65) Suppose that aging were caused by the accumulation of somatic mutations (changes in the DNA of cells other than primordial germ cells). * Then why would you have predicted that Dolly the cloned sheep would have died at an unusually young age? (As she did).

*66) Then what would you predict about statistical patterns of changes in death rates?

67) If Dolly and other animals produced by nuclear transplantation into oocytes turn out not to age sooner that animals born the normal way, what implications would that have for the idea that aging results from shortening of telomeres?

68) What about getting the nuclei from cells that have been living in tissue culture for various lengths of time? What ought to happen?
Hint: Maybe being put into an oocyte causes telomeres to increase greatly in length?

Question 69 was a duplicate and has been deleted.


70) All cells of the body contain all the enzymes and signalling proteins needed to cause the cell to digest itself from the inside out (apoptosis). Why should cancer researchers be trying to cause apoptosis in all cells that have any cancerous properties, as opposed to trying to inhibit DNA synthesis and mitosis in fast-growing cells

71) Why are lymphomas the only kind of cancer that can be cured using mono-clonal antibodies that selectively fit only the cancer cells?
Hint: Remember that each lymphocyte, including each cancerous lymphocyte, makes lots and lots of binding sites that all have the same shape as each other.

72) 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?

73) What are at least five frequently observed abnormalities of cancer cells?

74) For each of these five abnormalities propose a treatment for treating cancer.

75) Suppose that a drug slows down growth of normal cells, even to the point of stopping it, but doesn't slow cancer cells. How could you use this drug to kill cancer?
Hint: Why would it work even better if the drug speeded up the growth of cancer cells?

76) What are the distinctions between carcinomas, sarcomas, lymphomas and leukemia?

77) What are oncogenes? Give at least three examples, including the names of the genes and the type of protein they encode.

78) 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.

79) Why is blocking the activity of an oncogene not a cure for cancer?

80) How are checkpoint controls in the cell cycle related to cancer and to cancer treatments?

81) How might cancer be treated by a chemical analog of glucose that is poisonous?

82) Suggest a relationship between drugs that inhibit mitosis or DNA synthesis, and how they are related to killing faster growing cancer cells.

83) What does metastasis have to do with the importance of detecting cancers as early as possible?

84) 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?

85) 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.

86) Is apoptosis likely to be important in treating cancer? Why or why not?

87) 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.

88) What is the biological effect of cyclophosphamide? Why might cyclophosphamide be expected to produce effects similar to aging?

89) What is the biological effect of vinblastine?

90) Explain why it could be useful to have a drug that selectively stops DNA synthesis and mitosis in normal cells but not cancer cells.

91) Could such drugs also be useful if they affected cancer cells but not normal cells? If in doubt, explain your reasoning.


92) What was the name of the 19th century biologist who invented the once popular phrase "ontogeny recapitulates phylogeny"? Hint: Haeckel
What does this phrase mean?

*93) 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?
[I realize this is a difficult question but I would like to hear your answer.]

94) 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?

95) Causes of embryological phenomena can be divided into Genetic, and what other three categories?

96) Does embryology of some animals depend on some but not all of these, or do all animals have all of them?

97) If we had not evolved from fish, what would be different about our embryonic development?

98) 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

99) Why was it surprising that the Pax-6 gene controls location of development of eyes in insects and also in vertebrates?
Hint: think about the difference in the structure of the eyes in insects vs. vertebrates.

100) What does this suggest to you? Does it suggest that evolutionary changes in embryological processes occur faster than the amino acid sequences of signaling molecules, or the reverse, or what?