Midterm, signal transduction, Fall 2000
Print your name neatly here----->> * *
BL A512 -- Signal Transduction Fall -- 2000 -- Prof. Stark
Midterm Exam -- Tuesday, October 17 -- 100 points
1. Above is a diagram of a ligand gated G-protein signaling mechanism (Alberts
et al., Fig 15-14B). For pedagogical reasons, it is greatly oversimplified.
Suppose you are a college teacher presenting this material to undergraduates
for the first time in anticipation of further developing the topic with
more detailed diagrams. What are some of the first, most fundamental, things
you would say about (a) the molecule to which the ligand binds and (b) the
G-protein to prepare the students for that more detailed coverage? (3 points)
2. Above (Alberts et al., Fig. 15-1) is the figure used to introduce the
"cell signaling" chapter. The top would easily apply to an example
such as the beta adrenergic receptor. Describe the example given (so far
this semester) of the mechanism for which the bottom diagram applies. Describe
the molecular configurations of the signaling molecule and the receptor
for that example. (5 points)
3. If this were a voltage-gated sodium channel, describe the molecular nature
of the gating mechanism and what happens to this gating portion of the molecule
prior to the open state. If this were a voltage gated channel (use Shaker
as an example), describe the molecular nature of the inactivation mechanism
(3 points) (from Fig. 11-22, Alberts et al.)
4. (a) What is this molecule? (Alberts et al., Fig. 15-6) (b) What is the
precursor (in biological systems) of this molecule? (c) What enzyme splits
this molecule off from its precursor? (d) What is this molecule converted
to by the cyclooxygenase dependent pathway? (e) What drugs do people take
to affect this step? (5 points)
5. What is the whole molecule (to the left) and the particular properties
of that part of the molecule (to the right) to which the 4 cAMP molecules
(circles) are shown to bind? What should be added to this diagram after
the "+" sign? (Alberts et al., Fig. 15-24) (3 points)
6. Here is a channel (Hamill and McBride 1995, Fig. 9) shown to interact
with another membrane protein as well as some proteins housed intracellularly.
What type of channel is this? What is dystrophin and how does it come to
have that name? (3 points)
7. Here is a picture of connexin-32 indicating mutations causing Charcot-Marie-Tooth
disease. Draw a picture of how such proteins assemble in or near the membrane
and describe what the function and name of such an assemblage of protein
molecules is. (4 points) (Bergoffen et al., 1993)
8. Here is gene product of the cystic fibrosis gene. What does it do to
what ion? What is the NBF? (3 points) (Riordan et al., Fig. 7)
9. Shaker was cloned starting from the mutant. By contrast, the voltage
gated sodium channel and the nicotinic receptor were cloned quite differently.
How were these two cloned (starting how)? To which of these does shaker
most closely compare (structure of the protein) and what is the major difference?
(5 points) (Templ, Fig. 2)
10. Here (Jan and Jan Fig. 8) is a model we discussed, and it is replete
with jargons, some of which you were exposed to repeatedly. Translate "GIRK."
Give the pharmacological name of the Acetylcholine receptor shown. (4 points)
11. What does this tell you about what kind of receptor in Paramecium?
(3 points) (Eckert, 1972, Fig. 6, top right)
12. What is trp? What is the InsP3 receptor? (2 points) (Fig. 2.
13. Here (Alberts et al., Fig. 11-34) is an activated neuromuscular junction.
(a) What gates the channel marked "3" on the muscle cell membrane
away from the neuromuscular junction. (b) Given the information that "4"
is the transverse tubule, what is that channel? (c) Given the information
that "5" is the calcium channel from the muscle's internal reservoir,
what is the name of this reservoir? (3 points)
14. This (Wittinghofer, Fig. 2) is a schematic of the interaction of a receptor
with another protein complex. (a,b) If it were a rod, what would the receptor
and protein complex be called respectively? © If this were inhibitory,
where would ADP ribosylation by pertussis toxin take place? (d) Why are
2, 3, and C cross-hatched? (4 points)
15. Calcium is coming in through a channel to what natural ligand? What
keeps NOS near the NMDA-R? After NO leaves the cell, what is the main enzyme
it affects? (3 points) (Snyder, 1992)
16. This snippit from the vertebrate phototransduction cascade (Poulans)
shows GCAP. Where did the calcium come from? What process does calcium mediate
in vertebrate phototransduction? In Drosophila phototransduction,
what are the two sources of calcium? In Paramecium, what different
calcium binding protein was found to be mutated in pantophobiac mutants?
17. Here is a diagram of arrestin binding to rhodopsin subsequent to its
activation by light (Jindrova, Fig. 2). (a) What had to happen to (b) what
kinds of amino acids on (c) what part of the molecule on (d) what side of
the membrane before arrestin binds? (e) What enzyme did this to rhodopsin?
What enzyme would have done the same thing to the beta adrenergic receptor?
18. Here is the molecule that transducin activates in the rod. What is it?
After transducin activates it, how is it different from this picture? In
the rd (rodless) mouse, what is wrong with what part of this molecule?
When it is normal, activated and functioning, it converts what to what?
(6 points) (Farber, Fig. 1)
19. Here is "red vs. green" in the human opsin cloning paper (Nathans
et al., 1986, Fig. 11 D). What are the black dots and how would their number
compare for green vs. blue and green vs. rod rhodopsin? What is missing
in these old figures of G-protein-coupled receptors in terms of membrane
embedding? Luminal and cytoplasmic faces are shown. Where is the N terminal?(4
20. Here is a diagram of the olfactory transduction cascade, replete with
jargon (Molday, 1996). What is CaM and what does it look like molecularly?
What is CNGC and what does it look like molecularly? Fot the human, how
many different R's are there, and how are these coded in genes and chromosomes?
21. This snippit (from Kinnamon and Margolskee Fig. 2) shows a cAMP mechanism
for sweet taste. How does this differ from how the cyclic nucleotides affect
channels in rods. (4 points)
22. Here is a diagram pertaining to ras (Alberts et al., Fig. 15.53). How
does this GTP binding protein differ in its dealings with GTP/GDP from those
of the alpha subunit of the heterotrimeric G-protein? (4 points)
23. Here is a simplified diagram of a hormone mechanism (Mangelsdorf et
al., Fig. 2). If this were a steroid hormone, what are the major domains
of its receptor? If this were a retinoid mechanism, about how big is the
HRE and what is its configuration? (5 points)
24. Describe the function of this metabotropic glutamate receptor in the
taste receptor. (3 points) (Kinnamon and Margolskee, Fig. 2)
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