Review questions after third exam:

Vertebrate bodies (including humans) are made of about how many differentiated cell types?

In the life cycle of Dictyostelium there are how many differentiated cell types?

Name at least ten differentiated cell types, found in humans and other vertebrates?

Housekeeping genes are transcribed in which differentiated cell types?

What is the relation between transcription of "luxury genes" and cell differentiation?

How are stem cells related to cell differentiation? ("stem cells" in the older, traditional sense of that word)

What is the expectation or hope about the differentiation of "Embryonic stem cells" (in the new sense of the phrase "stem cell")

Contrast the meaning of "hemopoietic stem cell" to the meaning of "embryonic stem cells".

Is it possible for human cells to transcribe (all) the luxury genes normally transcribed of two differentiated cell types?

In terms of what you learned in earlier courses about the control of gene transcription (for example, in operons, cytosine methylation, or anything else, suggest a molecular mechanism for turning on the luxury genes of each particular differentiated cell types.
(hint: the promoter regions of each set of luxury genes might contain very similar base sequences, not found in the promoter regions of luxury genes of other differentiated cell types.)

Consider whether your hypothetical mechanism (for causing differentiation) would cause differentiation to be irreversible and self-perpetuating.

Suggest how your hypothetical molecular mechanism (for simultaneously turning on transcription of luxury genes) would prevent cells from differentiating simultaneously into two or more different cell types.

Can you add some ideas to your hypothesis that would cause cells not to be able to transcribe the luxury genes of more than one differentiated cell type?

What would your hypothesis predict ought to happen if two cells (each of a different cell type) were fused with each other?

(What really does happen is that both nuclei cease transcribing all the luxury genes of both differentiated cell types.)

An exception to this rule is what happens if differentiated cells get fused into (highly multinucleate) skeletal muscle cells. Can you suggest a logical reason for this?

Suggest an experimental test of this reason.

Tetraploid cells are how big (in volume) relative to diploid cells of the same differentiated cell type?

Tetraploid animals have about how many more, or less, cells in their bodies, as compared with diploid cells?

Haploid cells are how big (in volume) relative to diploid cells of the same differentiated cell type?

Haploid cells have about how many more, or less, cells in their bodies, as compared with diploid cells?

Explain why skeletal muscle cells are probably an exception to the rule (in these last four questions)
(Hint: why would osteoclasts probably also be an exception, for the same reason)

What is an example of metamorphosis in a vertebrate? (Conversion of a what to a what?)

What is an example of metamorphosis in echinoderms? (Conversion of a what to a what?)

What is an example of metamorphosis in insects? (Conversion of a what to a what?)

What is an example of metamorphosis in a kind of arthropod that isn't an insect? (hint: barnacles)

Besides the loss of their tails, what other changes occur during metamorphosis of tadpoles?

What hormone stimulates metamorphosis in frogs and salamanders?

How is molting of insects related to their metamorphosis?

Ecdysone is a steroid hormone that stimulates molting in insects and other arthropods: true or false?

Juvenile hormone inhibits metamorphosis from occurring when an insect larva undergoes metamorphosis?

* If you wanted to create Jabba The Hutt out of a fly maggot, how might you use juvenile hormone to accomplish that?   This question was revised April 24.

Review questions on the subject of the development of the immune system

The following is an exact quote from the NIH's "Medline" information web site:

"In patients with an autoimmune disorder, the immune system can't tell the difference between healthy body tissue and antigens."

Discuss what is misleading about this quote. What misunderstandings about the immune system is it based on? What fallacies does it pass along to readers?

Are there any consistent differences between body tissue and antigens?

Be prepared to discuss why or whether the misinformation in this quote is the reason why cures have not yet been discovered for Multiple Sclerosis, Lupus, Rheumatoid Arthritis and other autoimmune diseases.
(I promise to respect a good argument pro or con. But I confess to the belief that fallacies like this are much worse than simple ignorance.)

Here is another quote from the same medline "information" site:
"What causes the immune system to no longer tell the difference between healthy body tissues and antigens is unknown."

Besides the vulgarity of splitting an infinitive, what else is misguided about this sentence?

Is it correct about what is unknown? In what sense is it already known "what causes the immune system... no longer to be able to tell the difference..."

Is there really A particular, single difference between body tissues..."

Do antigens have particular properties capable of being distinguished from body tissues?

What do the (well-meaning) authors of the Medline web page assume about why the immune system attacks molecules of certain shapes?

What do they assume about what goes wrong in autoimmune diseases?

Can you write one or two accurate sentences to substitute for the ones quoted above?

If a scientist wanted to invent a cure for autoimmune diseases, would these quotes point them in the wrong direction; or rather, in what respects do these sentences point in the wrong direction?

If you could somehow magically get absolutely true yes or no answers to a series of questions about what causes multiple sclerosis, or some other autoimmune disease, what would these questions be?

According to the clonal selection theory, what two selections of what clones occurs,
A) when a person is infected by a germ?
B) when the immune system becomes permanently unable to make antibodies that fit "self" antigens?

Chemicals that stimulate "A" above are called "adjuvants" (which means helpers), and are often added to vaccines to make the work better.

Imagine a chemical or other treatment what would help the clonal selection event that I called "B" above.

What would be the use of an equivalent to adjuvants for the self-tolerance mechanism?

What is meant by VDJ recombination?

About what percentage of VDJ recombination events should result in the equivalent of a frame shift mutation?

Review questions on cancer

a) List and briefly describe at least eight common differences between cancer cells and normal (non-cancerous) cells of the same differentiated cell type.

b) What is the Warburg Effect?

c) Describe the decreased sensitivity of cancer cells discovered by Prof. Barbara Danowski, and shown in a video in class.

d) How is apoptosis related to cancer; and to the effectiveness of some anti-DNA chemotherapy drugs; and to possible future cures for cancer.

e) How might cancer be treated by a drug that is changed from being poisonous to being non-poisonous by becoming covalently bonded to phosphate groups.

f) How might cancer be treated by a chemical analog of glucose that is poisonous.

g) Why might the drug in the previous question be more effective if mitochondria could oxidize it to a non-poisonous form?

h) If a drug became poisonous when it reacted with lactic acid, how might that help it kill cancer cells?

i) In the context of cancer chemotherapy, what is meant by "spindle poisons"

j) In relation to cancer chemotherapy, what is meant by "nitrogen mustards"?

k) Although it is true that most chemotherapy drugs are especially harmful to fast growing cells (hair, bone marrow stem cells, intestine), explain how such drugs can often kill slow-growing cancers.
(Hint: remember check-point control mechanisms)

l) Describe abnormalities of cancer cells that you have seen in time-lapse videos, in photographs, and in Pathology textbook descriptions. (the more abnormalities you describe, the better)

j) What is the defining property of an oncogene?

k) What different kinds of normal proteins are coded for by oncogenes? (Name specific oncogenes, and then describe the function of the protein coded for by that oncogene). The more different kinds of proteins, the better.

l) Although nearly all mutagens (chemicals that can cause mutations) are also carcinogens (chemicals that can cause cancer), the category of carcinogens that cause "frame shifts" (gain or loss of a base pair from DNA) were reported to cause relatively few cancers - fewer than other kinds of mutagens.

What could have been deduced from this about how mutations cause cancer? (Hint: about what changes in proteins can cause cancer, as opposed to what kinds of changes in most oncogene proteins result in cancer)

m) List the name of six specific oncogenes; describe the normal functions of the proteins coded for by each oncogene. (I realize this is similar to a previous question; sorry; Please learn it twice)

n) Please describe the "chain of command" by which each of these oncogene proteins normally affect each other. (Hint: pass along signals)

o) 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.

p) What percentage of US citizens will be diagnosed with a potentially fatal form of cancer at some time in their life?

q) What fraction of US citizens die of cancer, currently.

r) What infectious disease used to kill an even a larger fraction of Americans and English than cancer does now?

s) Until about what year did this infectious disease kill more Americans and English than cancer did then?

t) What disease killed Thomas Wolfe and George Orwell?

u) Why did that disease become so much more curable than cancer?

v) Invent a new strategy for curing cancer.

w) Do cancer cells contain caspase enzymes, and other proteins capable of causing programmed cell death (= apoptosis)?

x) What is metastasis?

y) Describe the phenomenon of "contact inhibition" and the statistical data by which it was discovered.

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

This concludes the list of review questions. There will be no questions on aging or evolution on the exam

The final exam will contain questions from all parts of the course. Many of the questions will come from those earlier lists of review questions, so you should review all parts of the course.

Final course grades will be calculated as follows:

If you took all three hour exams, you can drop the one with the lowest grade. The final exam will then be 50% of your course grade, and the two remaining hour exams will count 25% each.

If your grade on the final exam is lower than any of your hour exam grades, then it will be 40% of your final grade, and the three hour exams will count 20% each.

Best of luck on the exam, and may you find ways to put this knowledge to use.


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