Biology 441, Spring 2014


Last set of review questions

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 this new one.

You are also responsible for the figures and illustrations posted on the course web pages.


How does sex determination work in Drosophila, and how is it different from sex determination in mammals? (Hint: both have X and Y chromosomes but the mechanisms by which sex is determined are very different. Be prepared to explain this.)

What controls whether turtle and alligator embryos will develop into males or females? What is unusual about sex determination in fish?

What tissues are the testis and the ovary and the sex ducts derived from?

What is the Müllerian duct? What is the Wolffian duct? What happens to them in embryonic development?

Where do the testes originate in development of mammals, and what happens to them during development? What is different about the position of the testes in birds?

What is another example of organ migration in mammals?

Contrast the internal histology of the testes and the ovaries.

What is meant by dosage compensation in mammals?

What is metamorphosis?

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

What are at least 7 different changes that occur when a tadpole metamorphoses into a frog?

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

What is ecdysone?

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

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

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

What is the biochemical mechanism of programmed cell death? (Hint: What is a caspase? Where are caspases normally located? Why are their active sites normally blocked? )

List as many specific examples as you can of apoptosis.

How was genetic research on the nematode C. elegans essential for the discovery of the biochemical cause of apoptosis?

Why was it important for the discovery of caspases in general that C. elegans coincidentally happens to have only one gene for a caspase, rather than 2 or more?

What are at least two connections between cancer and apoptosis?

If a drug activated caspases when stimulated by an over-active oncogene protein, would this be useful?

What is metastasis?

Compare and contrast the reversibility of differentiation in animal cells versus plant cells.

What is a specific example of regeneration in which cells convert from one cell type to another?

What is at least one example in which regeneration does NOT depend on cells changing from one cell type to another?

* 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?

* Invent a mechanism that might explain the (ususal) near-irreversibility of cytodifferentiation of animal cells.

* Extend your hypothetical mechanism to explain why animal cells cannot simultaneously belong to two differentiated cell types (i.e. express two different sets of luxury genes; e.g. simultaneously be a muscle cell and also a lymphocyte).

* What could be accomplished by fusing leukemia or lymphoma cells with cells of any other differeniateded cell type?

* Further extend your hypothesis to relate the molecular mechanism(s) of differentiation to the branching pattern of ectoderm, mesoderm and endoderm, followed by the subdivision of ectoderm into neural tube, neural crest, etc., subdivision of the mesoderm into notochord, somites, intermediate mesoderm & lateral plate mesoderm, subdivision of somites into dermatome, etc.

Describe the sequence of events that occur when a newt or other salamander regenerates one of its legs.

What is a blastema? What does dedifferentiate mean?

When salamanders regenerate the skeleton and musculature of one of their legs, do any of the previous chondrocytes redifferentiate as muscle cells?

What is some of the experimental evidence for or against this fact?

Likewise, do any of the previous muscle cells redifferentiate as skeletal cells? And what is some evidence?

Discuss why, or why not, you would or would not have expected these results, drawing on several particular facts and principles that you have learned in other parts of the course.

*What are some facts that would have led you to expect these results?

*Conversely, what facts would have led you to expect that dedifferentiated blastema cells would re-differentiate into whichever differentiated cell type is needed at each particular location. (Hint: You can use Wolpert's concept of positional information in your answer to this question).

In what ways is what happens in salamander limb regeneration like what happens when dissociated sponge cells sort out?

In what ways is salamander limb regeneration like when happens when embryonic vertebrate cells are dissociated and randomly mixed? (Hint: How are the behaviors of cartilage and muscle cells similar or different in sorting out as contrasted with what happens is salamander regeneration of limb skeleton and musculature)

Budding in Hydra requires (involves; is caused by) what changes in the curvatures of its surface (both the amounts and the directionality of the curvatures of its surface)?

Budding of Hydra needs what changes of directionality and/or amount of contractile tension in the body wall? (assume there is some fluid pressure in the interior "gastrovascular cavity", on the average, but that at no time does this inner pressure change from one location to another).

Again, in Hydras, compare the curvature of the surface of the tentacles versus the curvature of the main body of the Hydra.

* As tentacles form and elongate by rearrangements and reorientations of body wall cells, what changes in either the amounts or directionality, or both, need to occur? (assuming, as before, that there is some fluid pressure in the enclosed cavity)

important: Compare the limb bud development with development of the entire animal of sea urchins, frogs, and mammals. (Hint: What happens when limb buds, and embryos are split in two, or fused side by side?)

Also, compare or contrast the development of anterior-posterior axes in limb buds as compared with whole embryos.

Imagine an experiment in which somebody takes an early snake embryo, soaks a plastic bead in fibroblast growth factor, and then surgically implants this bead into the somatic layer of the lateral plate mesoderm, and the snake then develops a leg, with fingers and claws, at the location where the bead was implanted! What might this result tell you about the molecular changes in evolution by which snakes stopped developing legs? (Specifically, as opposed to what other molecular changes that could have produced this same result).

Suppose that at the one cell stage of an embryo, two chromosomes happen to break at locations between promoter regions of certain genes and the parts of those genes that code for the protein, and then each chromosome fragment rejoins incorrectly with the DNA of the other chromosome. If the genes are normally transcribed only in differentiated cells (and NOT in the same cell type), then what will happen as a result of this genetic transloation?

important: (difficult, but likely to be on the exam) If Dolly the sheep had developed from an oocyte injected with a nucleus taken from a lymphocyte (instead of a nucleus from a mammary cell), then supposing she really did develop into a sheep, what would have been the most important and interesting abnormality of this sheep?

Antibodies are synthesized by which particular kind of cells?

T-lymphocytes bind to antigens at a binding site called what?

Suggest why it's necessary that the great majority of lymphocytes undergo apoptosis. (Hint: Remember the randomness of the VDJ recombination of lymphocyte DNA! This is important!)

Which of the following is closest to the reason that people don't normally make antibodies against their bodies' own antigens?

    a) Because every molecule in the body is labeled with special molecules that are special for them, and which lymphocytes recognize as "self", in the sense of avoiding attacks or binding to any molecule with that "self" label.

    b) Genetic linkage prevents anybody who inherits the gene for the A antigen from also inheriting the gene for antibodies that bind to the A antigen, and likewise for every combination of antigens and antibodies.

    c) Transcription of RNA is selectively inhibited for any antibody whose binding site would fit any of a person's own antigens.

    d) Because some mechanism weeds out those V, D and J regions of DNA that would code for antibodies that would fit any of that person's own antigens.

    e) Some mechanism selectively kills, inactivates or sequesters all B and T lymphocytes whose combinations of V, D and J regions of DNA actually do code for antibodies (or T-cell receptors) that actually do fit any of that person's own antigens.

    f) When antibodies bind to antigens that are present in large enough amounts, then those antibodies are quickly filtered out of the blood.)

    g) Some other mechanism? Put it in your own words.

Explain each of the following newly-invented-just-for-this-exam (but really might work!) cures for cancer (your explanations can include criticisms or means to improve them).

a) A chemical analog to tyrosine, which is not poisonous itself, but is converted into a poison when enough of this chemical's many -OH side chains get phosphorylated (covalently bonded to a phosphate group). Hint; What sort of molecular abnormality could attach phosphates to them?).

b) A twenty-some amino acid peptide that can be cleaved in two to produce any amino acid sequence very similar in conformation to an amino acid sequence found in vaccines against measles, polio or whooping cough.

c) An analog to GTP (guanosine triphosphate) that binds to Ras proteins, but which in this bound state stimulates apoptosis unless its third phosphate is quickly cleaved off.

d) A chemical that de-represses caspase enzymes in response to disorganization of the cytoskeleton.

e) A chemical that inhibits one or more of the cell cycle checkpoints, thereby allowing mitosis to continue even if the chromosomes are not aligned on the spindle, or that allows DNA synthesis to begin regardless of damage to the DNA.

f) A chemical that kills cells in which the bcl-2 protein somehow becomes too concentrated.

g) A chemotactic attractant that stimulates migration of cancerous cells toward the direction of increased concentration of this substance.

h) A drug that speeds up DNA synthesis and/or mitosis more in cancer cells than in normal cells.

i) A drug that slows down DNA synthesis and/or mitosis more in normal cells than in cancer cells.

j) A drug that creates holes through plasma membranes wherever certain growth factor receptor proteins are over-active.

Which of these ten is most likely to be an effective cure, in your opinion? Which of the ten is least likely to be effective?

Please invent several more new methods for taking advantage of (1) The abnormalities observed in cancer cells, (2) The biochemical effects of oncogenes, (3) And the mechanism of apoptosis for the purpose of selective killing of cancer cells, while harming normal cells as little as possible.

What are the major weaknesses of current methods of cancer chemotherapy? (Specificity, or lack of specificity? Side effects? Failure to take advantage of apoptosis? The fact that many cancers are slow-growing?)

You should be able to write a few sentences about each of the following:

    thymus gland
    t-cell receptor
    generation of diversity
    autoimmune disease
    immune tolerance

Why do we need an immune system? What two differentiated cell types do the attacking?

Do they ever attack anything other than germs? 2 examples.

An "antigen" is any molecule that is selectively bound to by (what parts of?) proteins called what?

Which are made and secreted by what differentiated cells?

Virus-infected cells are induced to do what?

This is accomplished by what other differentiated cell type?

The "Generator of Diversity" accomplishes what?

What is unusual about the genes for antibody binding sites?

* In your opinion which is more surprising? That people EVER make anti-self binding sites, or that this doesn't happen much more frequently? Please explain your reasons for this opinion.

Explain why chemical analogs of morphogens ought to be very powerful "teratogens". (A "teratogen" is a chemical that causes birth defects)

Describe three key facts about aging. Which of the three surprised you, and why?

Describe at least two phenomena in the area of evo-devo that surprised you, and explain why.

What fact or phenomenon that you learned about in this course surprised you most? Briefly describe the phenomenon and the evidence supporting its occurrence.


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