More Study Questions for the First Hour Exam
Posted February 2, 2016
1) In sea urchin embryos, the primary mesenchyme cells form which tissue?
2) Primary mesenchyme cells originally develop from cytoplasm located around what location of the oocyte?
3) Please sketch a sea urchin embryo late during the process of gastrulation. On this sketch, label the locations of the blastopore, the blastocoel, the archenteron, the primary mesenchyme, the stomodeum and the animal pole. (Write each of these words, and draw an arrow from the word to the location of each of these structures.)
4) Be able to recognize a sketch of a sea urchin gastrula, label its parts (as in the preceding question), and tell what tissue or organ will develop from each of these parts.
5) Please sketch a frog or salamander embryo early in gastrulation, and label the blastopore, the animal pole and the vegetal pole.
6) Label the parts of the surface of an early amphibian gastrula that will differentiate into nerve cells. (This is not as difficult as it might seem)
7) Sketch an amphibian embryo at the end of gastrulation, and label the locations of the future nerve cells and the blastopore.
8) Sketch an ambphibian neurula stage embryo which has previously had some notochord embryo grafted into its blastopore. Label the neural tube, and the second second neural tube.
9) Suppose that this same identical effect could be produced by grafting the Hensen's node from a gastrulating bird embryo into the blastocoel of a salamander blastula stage embryo:
What result would you predict?
If this result actually did occur, then please list as many hypothetical interpretations as you can based on those results.
Hint: Remember about the evolutionary conservatism of many of the genes in which mutations cause structural abnormalities to form in embryos.
10) Suggest possible medical uses for some of those proteins (in the preceding question), in combination with undifferentiated "stem" cells.
11) Sketch the conjoined twins that would develop if a primitive streak developed a Hensen's node near its middle, which then separated into two Hensens' nodes that then moved ("regression of the node" away from each other, in opposite directions toward the two ends of the primitive streak. Explain your reasoning.
12) Sketch conjoined twins that would develop if two Hensen's node developed at opposite ends of the same primitive streak, and then these two nodes moved toward each other along this single primitive streak. Explain your reasoning.
13) Sketch conjoined twins that would develop if two primitive streaks developed very close together and parallel to each other, each with its own Hensen's node developing at the same end, and with both these nodes moving ("regressing") in the same direction. Explain your reasoning.
14) Sketch conjoined twins that would develop from two closely adjacent primitive streaks, each with their Hensen's node starting at the opposite end, and if these Hensen's nodes regressed in opposite directions, going past each other, each going along its own primitive streak.
15) Sketch conjoined twins that would develop if a primitive streak were Y shaped, with two Hensen's nodes located at the tips of the two upper arms of the Y, and these two nodes regressed toward each other, then merged at the center of the Y, and continued to regress together down the lower part of the Y shape.
16) Sketch conjoined twins that would develop if a primitive streak were V shaped, with two Hensen's nodes at the upper tips of the V.
17) Sketch conjoined twins that would develop if a primitive streak were T shaped, with one Hensen's node starting at the left end of the upper cross-bar of the T, and the other Hensen's node starting at the bottom end of the T, if the former node regressed from right to left across the top, and the other node regressed from top to bottom.
18) Which of these seven imaginary pairs of imagined conjoined twins would be mirror images of each other? Which of the seven would not be mirror images?
19) Try to deduce rules for the directions of movements of nearby Hensen's node that would cause conjoined twins to have mirror image reflection symmetry (as, in fact, they always do).
20) Conversely, supposing that you wanted to produce pairs of conjoined twins that are NOT mirror images of each other, what movements of their Hensen's nodes would produce that abnormal result (i.e. lack of reflection symmetry).
* 21) Suggest whether such events (that would result in lack of reflection symmetry) either (a) just never occur, because of some properties of Hensen's nodes, or (b) because such situations do occur, but somehow kill both embryos or © kill one or the other of the embryos, or (d) result in each developing twin pushing each other away away, so that eventually they are not conjoined.
*22) Why might you expect that two Hensens' nodes on the same primitive steak can only move (regress) in opposite directions, in contrast to Hensen's nodes on nearby (but separate) Hensen's nodes can only regress in the same direction as each other.
23) The photograph below shows a pair of what will be conjoined twins of chickens. In what part of their bodies will they be joined together (and explain your reasoning).
24) Which of the seven scenarios (listed above, for producing pairs of conjoined twins) would produce the anatomical pattern shown in this photograph? Please explain your reasoning.
*25) If Wolpert's theory of "Positional Information" (i.e. that locations of embryonic structures are controlled by monotonic diffusion gradients) were true, would it (A) tend to cause conjoined twins to be mirror images of each other, or (B) tend to prevent any closely-spaced twins from being mirror images of each other.
26) (which is also a hint about the preceding question) Why would there need to be either an abnormal maximum or an abnormal minimum produced in the concentration gradient of a morphogen chemical, in order to produce closely spaced mirror image twins? (in terms of the "Positional Information" theory).
27) Would the morphogen gradients be mirror images of each other?
28) When Spemann and Prösholdt induced formation of additional amphibian bodies, would you expect the induced bodies to be a mirror image of that embryo's normal original body?
*29) Does it confirm or contradict Wolpert's "Positional Information" theory if induced twin bodies are always mirror images? (Hint: joined by equivalent parts of the body; head to head, etc.)
*30) Would the same prediction be made by other theories, such as what? (Maybe organ "A" induces differentiation of organ "B", which in turn induces formation of organ "C", which induces differentiation of organ "D", which induces undifferentiated cells to differentiate into "E" cells? Would that sort of theory predict the sort of embryonic induction discovered by Spemann and his graduate student? Hint: If so, which tissue would be the most effective for inducing another embryo? Would the most effective be A, B, C, D, or E?
*31) On the other hand, using the concepts of Lewis Wolpert's "Positional Information" monotonic gradients, figure out how to discover which part of an embryo contains the high end of the morphogen gradient based on their relative effectiveness for inducing additional bodies. E.g. What does it suggest (in terms of the theory) that future notochord cells are the most effective inducers of secondary bodies. When in doubt, explain your reasoing.
32) Describe and sketch the geometric pattern of locations of Hox gene transcription during embryonic development.
33) Remembering back, again, to Wolpert's Positional Information Theory, can you figure out how use that theory to produce the "Colinearity" patterns of Hox gene transcription? Please give it a try.
34) On the other hand, what if cells that synthesize a given Hox gene protein becomes (as a result) able to influence or control which Hox genes will be transcribed in nearby embryonic cells. For example, what if a cell that has "turned on" hox gene #1 therefore stimulates transcription of hox gene #2; and also that those cells transcribing hox gene #2, stimulate nearby cells to begin transcribing hox gene #3 etc.
**35) (very difficult? But maybe you can figure it out) Suppose that cells detect which hox genes are transcribed in all the cells right next to them, and (for example) if a cell's neighbors right in front of them transcribe hox #2, but its neighboring cells behind them transcribe hox #3, then no change occurs. However if cells adjacent to the rear instead transcribe hox #9, then suppose that discontinuity stimulates cells to grow, divide, and change which hox genes they express in such a way that those transcribing Hox #N are always in between cells transcribing Hox N-1 and those transcribing Hox N+1.
The point is that obeying such a "rule of averaging" or "rule of continuity" could provide rationale for colinearity. Try to figure out how.
36) Please sketch at least five stages of embryonic development of sea urchin embryos. (Like the eleven stages that I drew on the Jan eleventh web page)
Please label the parts.
37) Please sketch at least four stages of embryonic development of human embryos (Comparable to the mammal embryo sketches on the Jan 11th web page.)
38) List as many differences as you can, between sea urchin development as contrasted with human embryology.
39) Please list as many similarities as you can between sea urchin development and human embryology
40) Sketch a cross section through the stage of development in which there is the maximum similarity between embryos of all vertebrates (Fish, amphibians, birds, reptiles and humans.
41) In this section, label the neural tube, the somatic ectoderm, the notochord, the somites, the endoderm. (Like my color drawing about half-way through the Jan 11 web page.)
42) Why are human egg cells triploid right after gastrulation?
43) What's the distinction between invagination and ingression?
44) In what sense is cavitation the reverse of ingression?
45) Increasing size and density of yolk in oocytes tends to result in gastrulating by ingression rather than invagination. (?) Is that true? What are some examples? Suggest possible reasons.
46) Is there a relation between yolk density and size and holoblastic versus meroblastic cleavage? What is that relation? Can you explain this relation in mechanical terms?
47) Is it accurate to say that (most mammal) embryos cleave like sea urchins but gastrulate like birds? If so, what are the reasons for these similarities and differences?
48) Please sketch a railway branching in the pattern in which vertebrate embryonic tissues subdivide into the three "primary germ layers", and then how each of these subdivides further into brain, etc. etc. notochord etc. etc. lungs. Draw and label as many sub-branches as you can.
49) Sketch the formation of somites from anterior to posterior. Into what 3 subdivisions does each somite separate?
50) If a mutation caused fifty somites (instead of the normal 32) to develop in humans, what abnormalities would this produce in the adult?
(Hint: Remember that somite cells disperse after aggregating, and that even in the fetus stages of development, somites have already dispersed.)
(Another hint: What controls where arteries will branch out of the aorta? What controls where sensory and motor nerves will connect to the spinal cord.)
51) [VERY IMPORTANT]: For every one of the photographs, drawings and diagrams on the lecture web pages, you ought to be able to write what it depicts, label the parts and explain their significance.
52) That is true even for the "Two kinds of causality" diagram.
53) Suppose that you needed to produce some pentagonal snow-flakes.
Imagine two alternative methods:
#1) Carve small plates of ice with a laser beam.
#2) Mix a small concentration of some chemical into water that changes how the water molecules pack together, in such a way that this molecular packing has five-fold reflection symmetry, instead of hexagonal packing.
Which of these methods corresponds to causality by pushing an object around a piece graph paper with your finger tips? Which of these methods (for making pentagonal snow-flakes) is more like pulling downward on one point of a piece of graph paper made out of rubber?
54*) The methods by which genes cause formation of anatomical structures is more like pushing sideways or pulling downward? Wolpert's "Positional Information" concept is more like which of the "two kinds of causality."
Hint: Is the effect of a mutation more like pulling downward at a different point;
or do mutations produce the equivalent of a change in the pressure of finger tips.
You can argue either side of this issue.
Please suggest why Wolpert's theory is so popular.
55) Are the locations of clouds, rivers and mountains determined by detection of latitude, longitude and altitude by air, water and rocks? Please give some arguments on both sides.
*56) What do you say to the claim that embryology is more difficult that genetics because DNA strands are one dimensional but developing tissues are three dimensional?
*57) Is that why Wolpert uses a two dimensional structure (The French flag) to help understand how genes control anatomy?
58) What are some kinds of fish that are not teleosts?
59) What are the major advantages of zebra fish for embryological research? (as many advantages as you can remember.)
60) What are the enveloping layer and the yolk syncytial layer? Do they become any particular parts of the fishes bodies? (hint, no; but explain why)
61) What are "deep cells", and what organs of the fish's bodies to deep cells develop into?
62) How is the neurulation of teleost embryos different from the neurulation of other kinds of vertebrates? Would you guess this difference has any relation to the enveloping layer? *HINT: Why might teleosts seldom or never have the birth defect called "spina bifida"?
63) Sketch at least 4 stages of the early embryonic development of frog and salamander embryos.
64) What is a major advantage of frog and salamander embryos for embryological research?
65) What is meant by embryonic induction? What Swedish prize was awarded to Spemann for discovering embryonic induction? Do you think he deserved a prize for tying a human hair around an amphibian egg at the one cell stage?
66) Which UNC professor first proved that embryonic induction occurs in nematode embryos?
67) (Guess) why many scientists considered that nematodes might probably NOT have any examples of embryonic induction? Hint: It's NOT because they don't have notochords.
68) [Hint] If Driesch had used nematode embryos instead of starfish embryos, why would he have reached different conclusions?
69) What very important fact about normal development was proven by that experiment of tying a hair around the one-cell stage embryo?
70) Why was it important to tie the hair at such an early stage of development, instead of at the blastula stage, for example?
*71) Why was it so difficult to discover that one of the proteins that stimulates neural induction is the "noggin" protein. ** Why might it have been better if induction had first been discovered in Drosophila fly embryos? Do you think induction does occur in fly embryos? Argue either pro or con or both.
72) If salami can induce formation of neural tubes, why does that increase the difficulty of finding out what the normal molecular signal is that causes induction in normal embryos (into which nothing has been implanted)?
68) Imagine that extracts of salami could induce differentiation of more bone, wherever you injected the substance, would ten thousand dollars be charged for pieces of salami? What about bone morphogenic protein BMP, as compared with SMP?
*69) Were those eleven million dollar per researcher "honor"aria paid in return for providing hard work and the deep knowledge needed to find proteins that induce bone formation? Or was it paid to keep the secret how easy it was?
70) Describe the method and result of Wilhelm Roux's famous "hot needle" experiment. What theory was this experiment designed to confirm?
71) In what ways was this experiment and its results a little different from what is usually said or assumed?
*72) What do you think might be the real reasons for the results of this experiment?
73) Remembering Lewis Wolpert's very popular theory that embryonic regulation is caused by if-not-linear-then-at-least-monotonic "morphogen" chemical gradients, in what sense do the results of Roux's hot needle experiment contradict and maybe even disprove Wolpert's theory? Hint: Would diffusion gradients not be prevented or at least distorted by the hot needle damage to cells? Shouldn't any kind of cell-cell signalling, including induction, have been visibly disturbed by the effects if the hot needles?
*74) Suppose that poking cells with hot needles had stimulated cells to send strong inductive signals and induce nearby undamaged cells to switch from differentiating into skin to differentiate into nerves, instead. After all, if tiny pieces of salami can do it, maybe heat-damaged cells can, also!
Describe what Roux would have observed, if hot needles had released inducing substances.
Figure out what his interpretation would probably have been.
Would Roux have been the discoverer of embryonic induction, instead of Spemann?
Or would such results have been uninterpretable? And would Roux perhaps just not told people about them.
Without being stimulated and guided by some kind of theory, can you either design experiments or interpret their results?
75) If you were going to repeat Roux's hot needle experiment:
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i) Why would you NOT use nematodes?
ii) What would be good reasons to use sea urchins, or some other echinoderms?
iii) What new phenomenon or principle could you reasonably hope to discover by repeating Roux's hot needle experiment?
iv) Would you need to invent some new theory in order to justify a grant to repeat Roux's experiment?
*v) Can experimental results tell you anything that you have not already guessed might be true?
76) Suppose that, before the discovery of co-linearity, somebody had invented a hypothesis that predicted the existence of hox genes and the geometric correlation between their location on chromosomes and the parts of the body where those genes are selectively transcribed (i.e. if the theory had predicted colinearity), then would scientists have looked for evidence sooner, and would nearly everyone have been convinced that the theory must be the true explanation why colinearity has evolved.
*77) What are possible reasons why some genes change so little in evolution?
Hox gene base sequences, actin and histone amino acid sequences are examples.
Does evolutionary conservatism result from almost any change being harmful?
Would that be because the optimum structure has already been evolved; so any change is for the worst?
Or could the reason be that harm is produced by having two or more slightly different molecular structures in the same body at the same time?
78) Describe gastrulation in birds.
79) Describe gastrulation in mammals.
80) In what sense is the first week of human embryology spent building a pre-embryonic structure to house, feed and produce the eventual embryo, where gastrulation, neurulation, somite segmentation etc, can then subsequently occur.
81) Diagram the three different ways that mammals can form identical twins?
*82) Why would you guess that elementary textbooks and Wikipedia assume that identical twins occur by separation of the first two cells?
*83) Invent a fourth possible way that identical twins might have occurred, based on your knowledge of normal early development.
84) Chickens are deliberately "bred" to produce abnormally big yolks, for people to eat. Suggest why a side effect might be an increase in the frequency of identical twinning, including more conjoined twins in those eggs whose yolks are only moderately larger that normal, but separate twins in those with the biggest yolks. (Such phenomena have actually been reported).
85) The names of newly discovered genes are often based on what about the appearance of animals in which the new gene is mutated?
86) What is meant by a genetic screen?
87) What is (are) some relation(s) between genetic screens and model organisms?
88) Why has the discovery of the bicoid gene been especially influential?
89) Mutations in "gap genes" produce what sorts of morphological abnormalities?
90) All gap genes, all pair rule genes, all hox genes and many segment polarity genes code for proteins whose normal function is to bind to what, and control what process?
91) What is meant by the homeodomain of hox proteins? Hint: they have 13 arginines and six lysines out of 60 amino acids. (if random, they should have only three of each).
92) Suppose that you could move (translocate) a mouse's hox b2 gene to the location between its hox b8 gene and its hox b9 gene, and also had fluorescently labeled RNA "probes" that would bind to the mRNAs for all of the hox b genes (b1, b2, b3, b4, b5, b6, b7, b8 and b9). (So that you would be able to see where in the bodies of mouse embryos each of these genes gets transcribed, and where it doesn't)
Explain what interesting results you would be especially interested in looking for, to discover where they occur. Hint: Regarding the causes and effects of colinearity. (And/or whatever other phenomena interest you).
*93) Increasing concentrations of retinoic acid (vitamin A) cause all hox genes to get transcribed slightly farther forward (to the anterior) in embryos, than normal. What does this mean? About birth defects? About "megavitamins"? About molecular mechanisms and functions of hox genes? About what controls where in the body hox genes get transcribed?
94) If any mutation in a certain gene causes very early death, even when heterozygous, then can that gene be found by a genetic screen? Hint: No. Please explain why such a gene is effectively invisible to genetic importance.
Also explain why evolutionary change in such a gene will be very "conservative" (Slow to non-existent).
95) If you dissect out small pieces of mesoderm from a developing embryo of a frog, bird or any vertebrate, and set it on the outer surface of another embryo (even of another species) then the mesoderm will often burrow into the other embryo and find its pathway to join and merge with the normal mesoderm. The equivalent can also be done by pieces of neural tube ectoderm.
What conclusion do such phenomena suggest?
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96) For example about the causes of gastrulation and neurulation?
97) About entelechies?
98) About that "two kinds of causality" diagram?
99) About the theory of "positional information"?
100) About regulative versus mosaic development?
About anything else you can think of?
The point is to display what you have learned so far in this course, and your ability to think originally about it.