Download (2 hour class period): 1) Reading quiz over multicellularity notes 2

In-class plan (2 hour class period):
1) Reading quiz over multicellularity notes
2) example: milk carton
a. Vitamin D Milk – why? Because Vitamin D is the precursor to a hormone
b. “This milk is from cows not supplemented with artificial growth hormones”
Talk about rBGH, its use and concerns, including IGF-1 levels
3) example: “BPA free” water bottles (estrogen-mimicking substances)
4) Ask the first set of in-class questions
5) Symmetrical vs asymetrical cell division. Both protein distribution and size/morphology
count: (different fates)
6) Make a point that oriented cell division can also give rise to asymmetry via which cells it
is now in contact with, or gradients, not just via autonomous signals (example: plant root
cell files: asymmetric division of the initials).
7) Ask the second set of in-class questions
At the beginning of the next class period, give a concept quiz over this material.
In class questions:
A
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Cell A secretes a diffusible signal. High concentrations of this signal stimulate cell division.
Which cell is more likely to divide: cell 1 or cell 2 (or neither)?
Cell 1
Now imagine that the signal produced by cell A that stimulates cell division is not secreted, but
instead remains attached to the plasma membrane and is thus displayed on the surface of cell A.
Now which cell is more likely to divide: cell 1 or cell 2 (or neither)?
Neither – only the cell touching cell A
What if the signal produced by cell A that stimulates cell division is an autonomous signal?
Which cell would divide?
Cell A
What if the signal produced by cell A that stimulates cell division is secreted, but instead of
freely diffusing it is an actively transported hormone? Now which cell (or cells) are most likely
to divide?
Can’t really say from this diagram, but perhaps all are equally likely (hormones not
generally used to specify positioning)
Different tissues respond in different ways to estrogen, and some tissues do not respond at all.
Why do you think that might be? (That is, what characteristics might control a cell’s response to
estrogen?)
Presence or absence of the estrogen receptor. The receptor itself could be an autonomous
signal, or the result of some other earlier signal that the cell received.
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You are studying the development of tiny animal. You find that at the four-cell stage, each one
of its cells is different, and will have a different fate. For example, the cell you call “1” will give
rise to all of the cells of the mouth (see top figure).
Now you do the following experiment: you pull cell 1 away from cell 2 and reattach it on the
other end, so that it touches cell four. Now when animal has finished developing it has a mouth
on its tail instead of on its head (see bottom figure). What does this tell you about the nature of
the signals that control the formation of this animal’s mouth?
They must be autonomous
Estrogen is a largely hydrophobic molecule. Which amino acid residues might you expect to
find in the part of the estrogen receptor that binds to estrogen? Name at least two, and the key
functional group of their R groups.
Hydrophobic amino acids, which have methyl groups – valine, leucine, alanine, etc.
Insulin is a small protein that acts as a hormone to regulate blood sugar levels. It is synthesized
in specialized cells in the pancreas. Due to their role as "professional secretory cells," these cells
have a very large endoplasmic reticulum and Golgi apparatus. They also have a mechanism that
triggers the secretion of the insulin they have synthesized when their ATP levels rise.
Why would insulin secreting cells need an unusually large endoplasmic reticulum and Golgi
apparatus?
Insulin is produced in the ER and must pass through the Golgi on its way to being secreted.
If the cells are making a lot of insulin, these compartments would need to be much bigger.
Why would it make sense for these cells to release insulin when their ATP levels rise?
When glucose is metabolized via glycolysis and oxidative phosphorylation, the end result is
ATP. Therefore, ATP levels in these cells are a good proxy for glucose levels.
Now think about the cells that respond to the insulin signal. What are some of the characteristics
would you expect these cells to have?
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An insulin receptor, connected to some sort of downstream signaling pathway
A glucose transporter that is somehow turned on in the presence of insulin (it actually
relocates to the plasma membrane)
A functioning glycolytic pathway, and something to do with the energy generated.
A young child has symptoms of diabetes (persistently high blood sugar), but produces normal
amounts of insulin. You sequence the patient’s genome, and find a mutation in the gene for the
insulin receptor. The mutant receptor will have a threonine instead of a serine at residue 1035.
Do you think that this mutation is likely to be the cause of these symptoms? Why or why not?
Name one other piece of information that you would like to have that would allow you to make a
better guess.
I didn’t actually end up using this one, but it might be a good challenging one.
Maybe. It would make sense in that if the mutation rendered the insulin receptor
nonfunctional, that would be expected to lead to symptoms of diabetes. However, not all
mutations make something non-functional. This is a relatively conservative mutation
(hydrophilic to hydrophilic), so it might not affect anything.
Another piece of information: Could be a lot of things, such as where this residue is on the
protein (e.g. is it near the insulin binding site?), or simply whether or not the receptor with
this mutation is functional.