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Bio154 Final-2006
Name: _____________________________
I.D. Number:________________________
TA:________________________________
Score:
1.__________(out of 12)
2.__________(out of 14)
3._________(out of 12)
4._________(out of 12)
5._________(out of 12)
6._________(out of 14)
7._________(out of 10)
8._________(out of 14)
Total:_______ (out of 100)
NOTE: Some questions may have multiple correct answers; as long as yours is
reasonable, logic and consistent, you can get full credit. Some questions may be
challenging but don’t panic; grading will be on a curve. Please try to be as concise as
possible. Almost all questions should be answered by one or two sentences. Good luck.
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QUESTION 1
A) After a long day of studying, you decide to go outside for a walk one night. Shining
your flashlight into the bushes outside your dorm, you see a silvery reflection out of the
eyes of a stray cat. Thinking of photos you have seen, you realize that shining bright
white lights (like camera flashes) into human eyes produces not a white/silver reflection,
but a strong red reflection (the dreaded “red-eye”). Why have many nocturnal predators
(like cats) changed the way light is absorbed by the retinal epithelium? (2 pts)
In nocturnal animals, their retinal epithelium reflects all the light back onto the
retina thereby increasing the light the retina sees, and thus improving vision under
low light conditions.
B) Walking a little further from the dorm, you come upon another animal, a rare
nocturnal salamander. Recognizing a cheap supply of experimental subjects, you take a
bunch of salamanders into the lab and begin to examine their rod responses. You begin
by recording the dark noise currents of single salamander rods, and compare the
responses to those of single rods in a related, diurnal (day-active) salamander (traces from
3 rods each are shown below). You choose to focus on the discrete events only.
Nocturnal
Diurnal
Summarize the differences between these two responses, and provide a plausible
mechanism for each. (4 pts)
Here we’re looking at discrete noise events. In the nocturnal animal, the discrete
events are more frequent (more of them in the same amount of time) and also
have a slower decay (they are broader).
The increased frequency of discrete events is probably due to an increase in the
spontaneous rate of activation of Rhodopsin, i.e., the spontaneous isomerization
of 11-cis retinal. This could happen if nocturnal animals have more rhodopsin
molecules or if they are less stable.
2
The events in the nocturnal rods could be slower due do sluggish recovery or
shut-off mechanisms. Plausible mechanisms would include:
 Less or slower rhodopsin kinase
 Less or slower arrestin.
 Transducin may inactivate more slowly due to slower intrinsic GTP-ase
activity or because they might be less RGS9 in the nocturnal rods.
 A slower guanylate kinase.
Give one advantage and one disadvantage that these adaptations confer upon the
nocturnal salamander? (2 pts)
Advantages: Increased sensitivity. Having more rhodopsin molecules (or less
stable) would make it easier for the rod to detect photons under low light
conditions. In addition, the responses stay “on” a little longer allowing for more
amplification of the signal.
Disadvantages: The system seems more prone to having spontaneous responses,
even in the absence of light stimulation, consequently there is more noise and the
system has a more difficult time sorting out true vs. false events.
Because the single rod responses are slow, the rods are less able to see rapidly
changing stimuli.
C) Extending your studies deeper into the retina, you examine the responses of single,
ON-center retinal ganglion cells to dim flashes, using light spots of different sizes.
Nocturnal
Diurnal
How do the receptive fields of ganglion cells differ between the two salamander species?
(1 pt) How does this difference make sense in terms of the single rod responses? (2 pts)
What is the disadvantage of this strategy to the nocturnal salamander? (1 pt)
The receptive fields of the nocturnal salamander are wider: This is shown by the
fact that for nocturnal salamanders you see the most activation with ~4 mm spot
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as compared to the diurnal salamander where the highest activity is seen with a 23 mm spot.
This makes much sense! We know that the rods in the nocturnal salamander a
more noisy, so it makes sense to compile more rods to figure out if the signal is
real and make sure is not is not coming from a spontaneous event in a noisy rod.
Making sure that the retinal ganglion cells signal only when several rods are
activated increases the fidelity of their vision.
The disadvantage of having wider receptive field is the loss of spatial acuity.
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QUESTION 2
A) 1991 marks an important year in olfaction research. Using molecular biology
techniques, Linda Buck and Richard Axel identified a large class of odorant receptors in
rodents. Please give two pieces of evidence used by Buck and Axel to argue that are
indeed odorant receptors. (2 pts)
Several answers were accepted.
A large and diverse family of GPCRs encodes olfactory receptors. The most
important part of this statement is that the family is very diverse, an important
feature when trying to encode the myriad scents of the natural world.
Olfactory receptors are expressed in olfactory epithelium, but not other somatic
tissues. Simply stating that ORs are expressed in the olfactory epithelium was not
sufficient for full credit; it was necessary to indicate that they are not expressed
elsewhere.
B) Having the large class of odorant receptors cloned allowed Buck and Axel to discover
two fundamental organizational principles of the olfactory bulb and epithelium. Describe
two principles and one method each that leads to the discovery of these principles. (4 pts)
Several answers were accepted, but it is important to recognize that the question
asks for organizational principles of the olfactory bulb and epithelium. This rules
out answers about ORN physiology, etc.
Each olfactory receptor neuron expresses only one olfactory receptor. – This can
be shown in a variety of ways: in situ hybridization, engineering mice to express
reporters in the same patterns as endogenous receptors.
ORNs expressing the same OR converge onto one of two bilaterally symmetric
glomeruli. – Again, this can be shown by in situ hybridization, by using a tauLacZ knockin to visualize axonal projections, or by targeting green fluorescent
protein to axons.
ORs are expressed randomly within a zone. – Although ORs are expressed
randomly within a zone, they are not expressed randomly within the olfactory
epithelium; full credit was not awarded without explicit reference to zones.
Again, this can be shown by in situ.
Note: Many other features of the olfactory system were discussed in lecture, but
these are not organizational principles of the olfactory system. While it may be
true that one odor activates a small number of ORs, or that ORNs adapt to a
sustained odor stimulus, these are not organizational principles.
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C) In 2006, Liberles and Buck found a new class of olfactory sensory neurons that
express another class of 7-transmembrane G-protein coupled “trace amine-associated
receptors” (TAARs). TAAR expressing sensory neurons are found to be distinct from
those that express conventional odorant receptors. To study the function of TAARs,
Liberles and Buck transfected individual TAARs into HEK293 cells, applied different
compound to the transfected cells, and assay for activity of a transcription reporter SEAP
(secreted alkaline phosphatase) (see Figure).
1. The SEAP is under the control of a cAMP response element (CRE) control.
Describe one possible signal transduction pathway between TAAR activation and
the SEAP transcription. (2 pts)
Must be in the correct order.
+0.5-G-protein
+1-any two of the following: AC, cAMP, PKA, PLC, PIP, IP3, DAG, Ca,
PKC
+0.5-CREB mediated transcription
2. From the data presented, draw one conclusion about the specificity of the TAAR
receptors? (2 pts)
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Any information that the type and number of compounds that they recognize gave
full credit.
D) Given the cloned TAAR receptors, describe two experiments to examine how
information is relayed from TAAR expressing neurons to their downstream neurons. In
other words, how are the TAAR neurons represented in the cortex? (4 pts)
1) Determine whether the axons converge onto specific glomeruli in olfactory bulb
+1
a. any mosaic technique +1
b. functional imaging of activity when exposed to different odorants
(intrinsic, calcium etc) +1
2) use trans-synaptic labeling to look at representation in cortex (Full credit was
given for trans-synaptic + anatomical experiments; most of the credit also give for
a combination of functional imaging in cortex eg fMRI, calcium etc in cortex and
anatomical study above in OB)
*If you got everything but the trans-synaptic labeling, give 3pts
*Only one except got 2 pts
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QUESTION 3
While doing a forward genetic screen in Drosophila for new circadian mutants, you
discover that one of your mutants is arrhythmic in constant darkness. After some diligent
genetics, you map the mutation to a gene which has not been previously described. You
decide to name your gene cadence (cad). Though nothing is known about this gene,
sequence comparison with known genes reveals that it has a predicted protein
dimerization domain, as well as a domain which may be involved with DNA binding.
Moreover, you raise an antibody against the gene and discover that the immunostaining is
usually nuclear.
A) One of the grad students in your lab who is working on cad tries to find out which
DNA sequence the protein may bind. After some work, your student reports to you that
cad is unable to bind DNA. This puts you in mind of other components of the circadian
clock. Which gene that we have studied does this new gene resemble, and what
mechanism of action does this suggest for cad? (2 pts)
a) period
b) transcriptional repressor
B) You decide to test your theory using the new antibody you have had made against
cad; you will stain fly tissue and observe localization and amount of cad. What
experiment will you do, and what do you expect to see? (4 pts)
The key to answering this question is to realize that the components of the
circadian clock that we have discussed in class cycle with respect to mRNA and
protein amounts. Because you will be using an antibody against cad, you will be
looking for differences in protein levels (intensity of immunofluorescence) and
localization at different times during the day/night (ZT) period. Acceptable
experiments included performing a western blot with samples harvested at
different ZT times from synchronized flies, immunohistochemistry, and
quantifying the amount of protein using an ELIZA.
Answers discussing the SCN were penalized (SCN is the mammalian pacemaker;
flies do not have an SCN).
Being an astute Drosophila researcher, you wonder if your gene is important for other
biological rhythms. After all, you are aware that other circadian genes are necessary for
some aspects of wildtype courtship song. Moreover, you know that some fruitless
mutants display altered courtship song, and that cad and fruitless are co-expressed in
some neurons. You wonder if the two cad phenotypes, circadian and courtship song, are
separable. That is, can a single fly display one phenotype while being wildtype with
respect to the other?
C) Assuming that these phenotypes are separable, what two experiment(s) can you
perform to demonstrate that they are? You have access to any fly stocks used in the
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paper from Manoli et al., as well as flies carrying UAS-cadence and UAS-cadenceIR (an
RNAi directed against the cadence gene product). For any flies you are examining please
describe their genotype with respect to fruitless, cadence, and any transgenes they may
carry. Also, please predict whether these flies will take the same length of time or longer
than wildtype to copulate, and whether they will remain rhythmic in constant darkness.
(6 pts)
If these two phenotypes are separable (as was given in the problem), a likely
explanation is that different populations of neurons underlie the circadian and
courtship song phenotypes. That is, if one population is mutant, the fly will
demonstrate either the courtship song defect or the circadian defect, but not both.
Therefore, the idea is to generate flies that are mosaics for cad function. This is
analogous to some experiments in the Manoli et al. paper. (e.g., Figure 4)
Experiment One
Genotype: cad -/-; fruitless P1-GAL4/+ (= wildtype); UAS-cadence
Males that are mutant for cad express both the circadian and courtship song
defects. Using fruP1GAL4, UAS-cadence, express cad only in cell that also
express fruitless P1 transcripts. These flies are mutant for cadence in all cells
except those expressing fruitless P1 transcripts. If the two phenotypes are
separable, one expects these males to become arrhythmic when switched to
constant darkness, but to have normal courtship song (and therefore will not take
longer than wildtype to copulate).
Experiment Two
Genotype: cad +/+; fruitless P1-GAL4/+ (= wildtype); UAS-cadenceIR
This experiment is the converse of the first experiment: instead of rescuing cad
function in a subset of cell, cad function has been disrupted. By driving the UAScadenceIR with the fru P1-GAL4, it is possible to eliminate cadence function in
only the cells where cad and fru overlap. One expects these males to remain
rhythmic in constant darkness, but to have a longer time to copulation (relative to
wildtype) because of defects in courtship song.
Variations: The only acceptable variation on the above experiments was to use
cadGal4 to drive UAS-fruMIR and “UAS-fruM.”
Note: Driving UAS-fruMIR with fruP1-GAL4 leads to males that do not court;
other perturbations of the fruitless locus can have the same effect. Because the
males must court to be able to score whether the two phenotypes are separable,
these experiments are not possible.
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QUESTION 4
The year is 2030. We have now discovered a set of drugs that will make stem cells
differentiate into cells that look like neurons—they are able to extend axons and dendrites
in vitro. Scientific researchers are just beginning to experiment with adding these stem
cell derived neural precursor cells into the adult brain to treat degenerative disorders. As
a medical researcher, you are particularly interested in using this type of therapy to treat
Parkinson’s Disease.
A) From what you learned about the pathology of the Parkinson’s disease, where in the
brain would be the most obvious place to put these stem cell derived precusors to treat
Parkinson’s Disease? (1 pt)
Substantia nigra pars compacta (+1)
Substantia nigra (+0.5)
Basal Ganglia (+0.25)
B) If you added these neural precursors into the adult brain and the patients don’t recover
movement control, give two possibilities about what else might have gone wrong? Give
one experiment to test whether this was a problem. Note: the precursor cells survive in
the brain and do not cause cancer. (4pts)
1) What went wrong? (+1 for each)
a. Guidance disrupted because cues aren’t present in adults
b. No functional connections
c. No release of dopamine
2) Experiment to Test (+2)
a. Anything feasible got full credit
*Credit also given for answers that implicated Parkinson’s genetic disorder,
PARKS, alpha synuclein if that addition of neural precursors would not overcome
the effect of predetermined genetic condition
C) It has recently been discovered that you can couple axon guidance molecules to small
beads. These beads can be placed in the brain without causing physical damage. To
repel axons of neural precursors away from a bead, what molecule should you attach to
the bead? To attract neural precursors, what molecule should you attach?
Note: it has been demonstrated that these stem-cell derived neural precursors
express Robo and Dcc, but not Unc5. (3pts)
Slit for repulsion (1.5) Netrin for attraction (1.5)
+0.5 if only said the molecule and not which process if was involved in
Sema, Eph, and Comm got no credit (receptors aren’t present in precursors)
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Cortex
1
Striatum
Thalamus
ACh
D1
4
2
11
D2
3
5
SNPC
9
10
GP (external) /
Subthalamic
Nucleus
8
6
STN
7
Globus Pallidus (internal) / Substantia
Nigra (pars reticular)
D) Given the numbered regions above, provide one region where you would put repulsive
beads in the brains of Parkinson’s patients? One region where you would put attractive
beads? (4 pts)
Repulsive beads—5,4,7,8,9,10,11 (not cortex because too far away)
Attractive beads—2,3,4
Big picture—put the beads to guide the precursors from SNpc where they have
been placed (see A) to D1 or D2
*Names, not # got 3pts
*For regions that if activated/inactivated would alleviate Parkinson’s symptoms,
no credit was given because it is unlikely that addition of the attractive/repulsive
beads would have any effect on adult neurons
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QUESTION 5
Sound pressure fluctuations result in displacement of a membrane in the auditory cochlea
such that different frequencies are represented as shown in the figure below.
A) Is auditory representation of sound frequency DISCRETE OR CONTINUOUS and is
this representation more similar to VISION OR OLFACTION? (2 pts)
1 pt: Continuous
1 pt: Vision
B) When adults who are congenitally or prelingually deaf receive cochlear implants, the
results are disappointing. They never gain language competence and often request that
the implant be removed. In contrast, early cochlear implantation in congenitally or
prelingually deafened children can lead to nearly perfect acoustic communication and
language competence. What may explain this phenomenon, based on our knowledge of
the development of the visual system? (1 pt)
1 pt: Critical period OR activity-dependent plasticity occurring within a limited
time frame early in development.
0.5 pt: Activity-dependent plasticity.
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In congenitally deaf cats, the CNS is deprived of acoustic input because of degeneration
of sensory cells before the onset of hearing. However, primary auditory afferents survive
and can be stimulated electrically by means of cochlear implants. Cochlear implants
when placed in both ears at the appropriate time is effective in allowing congenitally deaf
kittens to respond to different frequencies of sound.
C) Design an experiment with an appropriate control to determine when, after birth,
cochlear implants placed in both ears will be effective in congenitally deaf kittens. (2
pts.)
1 pt: Cochlear implants at different time points looking at behavior or cortical
imaging/electrophysiology.
1 pt: Negative control could be no implant, implant without turning on, fake
surgery. Positive control could be cochlear implant from birth on.
D) Name two ways you can map the receptive field properties of neurons in the auditory
cortex of kittens. (2 pts) What changes would you expect in the auditory cortex map of
congenitally deaf kittens that received cochlear implants in both ears at the appropriate
time compared to congenitally deaf kittens who did not receive cochlear implants? (2 pts)
2 pts: Any two of the following:
- Electrode recordings from cortex when giving sound (you could have said sound
coming from one direction, sound at different frequencies, sound at different
intensities… these different sound protocols were considered each as individual
answers so any 2 would count as 2 pts)
- Voltage-gated sensors
- Calcium sensors
- Transynaptic markers
2 pts: Enlarged auditory cortex in deaf kittens with cochlear implants compared to
deaf kittens without cochlear implants. More patterned/frequency tuned auditory
cortex in deaf kittens with cochlear implants compared to deaf kittens without
cochlear implants.
- 1 point only if you said auditory cortex columns (columns have been
shown in cortex to be present before sensory stimuli; spontaneous activity
is sufficient to induce column formation)
E) What do you think would happen to the auditory cortex map of congenitally deaf
kittens if the cochlear implants in both ears allowed transmission of only one frequency?
(3 pts)
3 pts: More uniform auditory map and increase representation in cortex toward
that one frequency.
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QUESTION 6
The neuromuscular junctions in C. elegans utilize the same excitatory neurotransmitterreceptor system compare as their vertebrate counterpart. In order to understand the
molecular mechanisms of synaptic transmission, aldicarb was used to perform a genetic
screen. Aldicarb causes paralysis and eventually death.
A) Use one or two sentences to explain the action of Aldicarb. (2 pts)
Aldicarb is a Acetylcholine Esterase (AchE) inhibitor. By blocking AchE activity
(essentially blocking the break down of Ach), an accumulation of Ach builds up in
the synapse and causes severe muscle contraction (paralysis) in the worm.
Partial credit if the student didn’t mention that Aldicarb blocks AchE specifically, or
if they didn’t state that an accumulation of Ach occurred in the synapse.
B) A forward genetic screen was performed to isolate mutants that are resistant to
Aldicarb induced paralysis. A number of mutations were isolated through this screen.
Among the genes that should be uncovered by this screen, list 4 genes that functions in
the presynaptic terminal and use one sentence to support your prediction for each gene. (4
pts)
Answers will vary here. Partial credit was given to the student that didn’t give an
explanation of the genes (or if the explanation was not good enough). Partial credit
was also given if the genes were too early in presynapse formation or if the mutants
realistically would not have showed a resistant phenotype to Aldicarb. No credit was
given to post-synaptic proteins.
C) You just found a new mutation in this screen and it appears to be dominant
(heterozygous animals showed a resistant-to-paralysis phenotype). After months of hard
work, you finally identified the mutation in a gene (you have just cloned it!). By
comparing the primary sequence of the gene to homologs in other species, you predict
that this gene encodes a potassium channel. What region of the protein is most indicative
that this is a potassium channel (not other channels)? (2 pts) Give a one-sentence
explanation why this is? (2 pts) How does the mutation affect the function of this protein?
(2 pts)
2 points: The ion selectivity pore is most indicative. (1 point given for p-loop).
2 points: This is the most conserved region among potassium channels.
2 points: Makes the channel constitutively active (always open).
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D) To study the function of this protein, you generate a knockout allele of this gene, this
time the mutation appears to be recessive. Can you predict what kind of phenotype you
will have on an Aldicarb assay and why? (2 pts)
This is a loss of function mutation of the K+ channel. Because these channels are
important for maintaining the negative resting membrane potential, without them
the membrane will be more depolarized and therefore hyper-excitable. Therefore,
the animals will be hypersensitive to Aldicard and they will show paralysis.
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QUESTION 7
In October of this year, Suo et al. came out with a publication that investigated the starvation
response in C. elegans. They noticed an alteration in the worm’s behavior as well as a metabolic
adaptation for survival. Their first key result was that starvation induced cAMP response
element-binding protein (CRH-1) activation in a specific set of neurons called the SIA neurons
(Fig 1. A&B).
Figure 1
SIA
A) What is the most likely genetic tool that the authors utilize here to image this activation in
live animals? (Although tzls is the background of the animal, it will not help you with your
answer). (1 pt)
A GFP fusion to the CRE promoter (CRE::GFP). (Also can be “reporter fused to
downstream target of CREB” for full credit.)
Students should know that they are trying to image in LIVE animals here. Tissue
staining, or techniques that use sacrificed animals, will get no credit. Calcium
imaging and FRET analysis are not the “most likely” technique used here for
analysis. Partial credit for “GFP fusion…” unless the wrong fusion was specified
(ie something upstream).
The authors go on to find that if the animals are fed the bioamine octopamine (which is found
endogenously in the animal) with their normal bacterial diet, the following results are seen (Fig
2. A&B). However, if they ablate the upstream neurons (MIA) and starve the worms, the effect
of octopamine is still present (Fig 2. C&D).
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Figure 2
+food
SIA
-food
MIAabl
MIAabl
B) What role do you hypothesize octopamine is playing in this system? (1 sentence, 1 pt)
Octopamine is the neurotransmitter activating he SIA neurons.
Full credit if the student didn’t use neurotransmitter but said that octopamine
acted directly on the SIA neurons. Partial credit if the student said “activation of
the starvation process” or “activation of CREB”.
You decide to continue this research and find two interesting mutants: ser-3 appears to contain a
loss-of-function mutation (unfed worms do not exhibit starvation phenotype) and egl-30 appears
to have a gain-of-function mutation (fed worms appear to be in starvation mode constitutively).
You find that these two genes encode SIA neuron specific proteins that bind to one another in
vitro by using coimmunoprecipitation and western blot assays. You want to further understand
the function of these two genes in vivo so you take a pharmacological approach. You feed these
mutant worms forskolin (a drug that activates adenylate cyclase) thus promoting the cellular
levels cAMP. After forskolin exposure you measure CRH-1 activation (indicated by + or -).
The following results are seen (Table 1).
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Table 1
Food
Forskolin
WT
ser-3lof
egl-30gof
ser-3lof, egl-30gof
Y
N
+
+
N
N
+
++
++
Y
Y
+
+
++
++
N
Y
++
+
+++
+++
C) With these data, you can tell that ser-3 lies UPSTREAM / DOWNSTREAM of egl-30 (circle
one). How do you know this? (4 pts)
The gene ser-3 lies UPSTREAM of egl-30.
This is credited to the double mutant results. Since ser-3lof; egl-30gof phenocopies
the egl-30gof mutant alone, one can tell that egl-30 is further downstream than ser3. Partial credit if the reasoning was correct but the word circled was incorrect
(logical thinking but ultimately incorrect conclusion).
D) Using your answer from part C, the co-IP data and western blot analyses, what proteins do
you think ser-3 and egl-30 encode? (2 sentences, 2 pts)
ser-3 encodes a GPCR and egl-30 encodes the downstream G-protein.
The addition of forskolin forces you upstream of the adenylate cyclase protein.
Hypothetically, any addition of forskolin to downstream mutants would have
altered the single mutant data in Table1. Therefore, students should write the two
upstream components that were extensively covered in class that are known to
bind (from the Co-IP and western blot info). Using the data from question (C), it
is known that ser-3 is upstream of egl-30. Partial credit if the student got one of
the proteins correct (even if it was reversed, ie ser-3 is a G-protein).
You find a new mutant, unc-13 (unfed worms fail to show a starvation phenotype). You
accidentally drop some of these mutants on a bacterial plate that has been supplemented with
octopamine. You’re curious and decide to look at these worms even though your PI tells you to
just chuck them out. Surprisingly, these worms now have the starvation phenotype!
E) Why do you think this is? What kind of process could unc-13 be mediating? (2 sentences, 2
pts)
unc-13 is mutation in a protein necessary for exocytosis at the presynapse and
keeps octopamine from being released from the upstream MIA neurons.
Full credit for any answer that suggested a decrease of octopamine
release/synthesis/etc. from/in the upstream neurons. Partial credit for simply
indicating that unc-13 is functioning upstream of octopamine since the question
asked for the kind of process that was being mediated.
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QUESTION 8
You have found a new exotic animal that has neurons with the following properties:
Vrest = 0 mV
[X+]out < [X+]in
[Y+]out >> [Y+]in
[Z-]in <<< [Z-]out
A) At resting potential, X+, Y+, and Z- are the only permeable ions. At resting potential,
does the chemical gradient of Y+ drive it in or out of the cell? (1 pt) What mechanism
does the neuron use to maintain the ionic concentration? (1 pt)
1 point: Into the cell.
1 point: Ion pumps.
B) You apply a neurotransmitter to this neuron which activates a channel, allowing X+ to
pass through the membrane. Does the membrane potential increase or decrease? (1 pt)
1 point: Decrease.
You allow the neuron to return to resting potential. Then you apply another
neurotransmitter to the neuron which activates another channel, allowing Y+ to
pass through the membrane. Does the membrane potential increase or decrease?
(1 pt)
1 point: Increase.
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C) While studying this cell, you find three channels that are selectively permeable for
each ion. You perform patch clamp experiments to obtain the I-V relationships for these
three channels. Based on the following I-V curves, which channel passes which ion? (3
pts) Give a 1-2 sentence explanation for each channel. (3 pts)
1 point for each correct pairing, 1 point for each explanation.
On an I-V curve, Eion is where the curve crosses the X-axis.
Channel A passes Z-. Given the ion concentration, EZ is very negative (Nernst
Equation). This graph shows the most negative Eion.
Channel B passes Y+. This graph shows only positive Eion. Also accepted: At
resting potential of 0mV, this is the only graph showing negative current (Y+
flowing inward).
Channel C passes X+. This graph shows a slightly negative Eion (less negative
than Channel A).
D) Which channel or channels are likely to be voltage-gated and why? (3 pts) Which
channel is likely to contribute most to the resting potential of this cell and why? (1 pt)
3 points for a completely correct response. Partial credit was given for lucky
guesses, and points were deducted for incorrect reasoning.
Channels A and B are likely to be voltage-gated because their I-V curves are nonlinear. This shows that the conductance changes with voltage.
Channel C is not voltage gated because it has a linear I-V curve, showing that its
conductance does not change with voltage.
1 point for the correct channel and explanation. 0.5 point for correct channel.
Channel B is likely to contribute most to the resting potential of this cell because
it has the greatest current at the 0mV resting potential.
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