Embryology   Biology 441   Vertebrate Embryology, Spring 2016   Albert Harris


Review questions for the last part of the course - part three

Review the embryology words at the beginning of the review for the second exam.

Briefly describe key experiments done, or embryology-related concepts proposed, by each of the following people:

    Wilhelm Roux
    Hans Driesch
    Ross Harrison
    Hans Spemann, and Hilde Prösholdt
    H.V. Wilson
    Hans Holtfreter
    Lewis Wolpert
    Alan Turing
    John Saunders

What combination of forces inflate the roof of vertebrate brains into a series of large "semi-spherical" bulges? Why is it not necessary for pressure to vary from place to place inside the brain and spinal cord? Why is it also not possible for outward pressure to vary from place to place in the brain and spinal cord. How might you reasonably hope to measure difference in pressures and tensions in different parts of an embryonic vertebrate brain? Can suction with a pipette measure amounts of tensions in different parts of an embryonic brain?
(Hint: what about directional variations in tension?)

Squeezing or stretching bone causes creation of temporary voltages:
What are two possible causes?
Hint: one of them is electrosmosis and the other one starts with the letter p.

Do electric fields have any known effects on the crawling locomotion of human body cells. Do the electric fields have to be DC or AC to produce these effects?

Regarding those the electric fields that can be produced by exerting physical forces on bones: Are those electric fields DC or AC. (Answer: AC. Can you explain why?

By what tissue grafts or other surgical disturbances can vertebrate limb buds be caused to branch into two limbs? How can you cause them to branch into three limbs? How did John Saunders cause chicken wing buds to graft into four wings?

In all these cases, the extra legs and wings are mirror images of each other: Does this mirror image symmetry suggest anything to you about the causal mechanisms?

When salamanders regenerate a leg, are the newly-formed muscles derived from mitotic descendants of cells that were already muscle cells before the amputation? Alternatively, do muscles develop from cells that had previously been part of the limb skeleton? Or are the new muscles formed from stem cells that had not yet differentiated until after the amputation? What evidence would persuade you of the answer to this question?

What about skeletal cells? When a salamander regenerates its front leg, do the new finger bones, radius and ulna etc. develop from previously undifferentiated stem cells, or are they formed by rearranging cells that had previously been been part of the humerus?

What are at least five normal functions of programmed cell death (apoptosis)?

The protein bcl-2 has what effect on programmed cell death? How was bcl-2 discovered, and how is this method of discovery related to the name?

What are caspases? How are they related to programmed cell death?

What is the distinction between necrosis versus apoptosis?

What process that occurs during insect metamorphosis is related to "hox genes", and to the discovery of hox genes?

What is ecdysone? (A steroid hormone in what kinds of animals that stimulates what process?)
(Hint: the answer is not simply "metamorphosis")

Multiple Sclerosis differs from most other autoimmune diseases in that both B and T lymphocytes have anti-self binding sites (with the same shaped binding sites as each other!) How could the develop the same shape?! (Remember that entirely different pieces of DNA are spliced to produce binding sites in B lymphocytes as in T lymphocytes. So what does it tell you, or what possible explanations are disproven by this surprising discovery that people with MS have antibody binding sites and also T-cell receptors that bind to the same "self" antigens?
Hint: How did these anti-myelin protein B and T lymphocytes both escape being weeded out?

The autoimmune disease "lupus" is caused by having antibodies specific for several different self molecules (histones, collagen, RNA, among others. Progress (worsening) of this disease sometimes includes development of more kinds of B lymphocytes that make antibodies against additional self molecules. What does this suggest to you about what goes wrong with the immune system that would explain (would have lead you to predict) production of multiple, and increasing numbers of anti-self antibodies?

Imagine that one autoimmune disease was caused by reactivation of the random DNA splicing enzymes, later in life, after birth. By what evidence, or peculiarities, of this disease could you detect that this abnormality is the likely cause of this disease?

Imagine a second, very different, autoimmune disease, that is caused by some particular "self" molecule being much more concealed from the tolerance mechanism, that weeds out both B and T lymphocytes whose binding sites fit that hidden self molecule. By what unusual properties of this disease could you deduce what goes wrong in its causation?

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

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).

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).

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

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?

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?

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

The currently proposed billion dollar "war on cancer" would allocate
A) more?
B) much more?
) about the same? D) less?
E) much less?
money than is being spent (per year) treating cancer patients?

Is there any way that average citizens could know this answer?

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

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

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?

The molecular mechanisms of penicillin and other antibiotics were not discovered until ten years or more after these drugs were themselves were discovered. Does that mean the discovery was accidental? What lesson can we learn from the true story of the discovery of antibiotics?


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