QUIZZES Flashcards
Very high concentrations of ADF/cofilin reduce the velocity of Listeria motility in the reconstitution assays of M.F. Carlier. Why is this? Choose the best answer.
Because too much ADF/cofilin destroys the actin network.
Because ADF/cofilin “unwinds” actin filaments.
Because ADF/cofilin has some affinity for ATP and ADP-Pi actin
Because ADF/cofilin is an actin-depolymerization factor.
Because too much of anything is a bad thing.
Because ADF/cofilin has some affinity for ATP and ADP-Pi actin
How can you make a “dominant active” form of a Rho family GTPase? Below are 5 ways you could change the behavior of a Rho family GTPase. Which of the 5 ways would make the Rho family GTPase “dominant active”. Select all that apply.
Make it so that the Rho family GTPase can’t hydrolyze GTP
Make it so that the Rho family GTPase can’t bind to its GAP
Make it so that the Rho family GTPase can’t bind to its GDI
Make it so that the Rho family GTPase can’t bind to its GEF
Make it so that the Rho family GTPase has very high affinity for its GEF
Make it so that the Rho family GTPase can’t hydrolyze GTP
Make it so that the Rho family GTPase can’t bind to its GAP
Make it so that the Rho family GTPase has very high affinity for its GEF
Consider a mutation in kinesin that increases its basal rate of ATP hydrolysis, where the basal rate is defined as the rate of ATP hydrolysis in the absence of any condition that might increase the rate of ATP hydrolysis, such as strain. What is the predicted effect of this mutation relative to wildtype kinesin?
a) The mutant kinesin walks faster on microtubules (increased velocity)
b) The mutant kinesin walks slower on microtubules (decreased velocity)
c) The mutant kinesin walks farther on microtubules (increased processivity or run-length)
d) The mutant kinesin walks less far on microtubules (decreased processivity or run length)
D
When a severing enzyme is added to taxol-stabilized microtubules attached to a cover glass, the severing enzyme cuts the microtubules into pieces. How could you prevent the severing enzyme from cutting the microtubules? Select all that apply.
Note: “preventing cutting” means that the number of severing events observed per unit time is reduced. “taxol-stabilized microtubules” are just microtubules that were polymerized and then stabilized with the drug taxol so that they do not undergo catastrophes.
a) Add the severing enzyme is a buffer that does not contain GTP.
b) Pre-treat the microtubules with an enzyme that removes the C-terminal “tails” of tubulin via proteolytic cleavage. (In other words, the enzyme cuts off the tails!)
c) Add the severing enzyme in a buffer that does not contain ATP.
d) Pre-treat the microtubules with a chemical cross-linking agent like glutaraldehyde, which will create covalent bonds between tubulins.
e) Add the severing enzyme in a buffer than also contains EB1.
BCD
Consider a mutation in tubulin that alters how tubulin changes its conformation after GTP hydrolysis. More specifically, the mutation makes tubulin “stiffer” after GTP hydrolysis, such that the tubulin does not transition as quickly between the straight and curved conformations. How would microtubule dynamics be affected by this mutation? Select two correct answers.
a) Microtubules will grow faster (the net growth rate increases).
b) Microtubules will shrink more slowly after a catastrophe (the “post-catastrophe shrinkage rate” is reduced).
c) Microtubules will undergo fewer catastrophes (the “catastrophe frequency” will decrease) and/or it will undergo more rescues
d) The GTP cap will be smaller
BC
Which analogy between actin binding proteins and microtubule binding proteins does not work?
Profilin : MCAK.
myosin : kinesin.
cofilin : katanin
XMAP215 : formin.
Arp2/3 : γ-TURC.
Profilin : MCAK.
Complexin is critical for the function of synapses because…
a) Complexin enables synaptic vesicles to be docked at the synaptic terminal membrane prior to Ca2+ influx
b) Complexin forms a complex with the v-SNARE/t-SNARE pair
c) Complexin is displaced from the v-SNARE/t-SNARE pair by synaptotagmin
d) v-SNARE/t-SNARE pairs are responsible for membrane fusion
e) Synaptic vesicles components are recycled
A
What is the cause of scurvy?
a) Fibronectin is not properly hydroxylated
b) Procollagen is not successfully cleaved into collagen
c) Yar! Too many Torrent downloads
d) Collagen propeptides do not form stable procollagen bundles
e) A diet low in citrus
D
Select all that apply.
Which of the following changes in receptor tyrosine kinase (RTK) signaling will cause cancer?
a) Shift the equilibrium of the extracellular domain toward the ligand-bound conformation
b) Production of truncated RTKs that lack their intracellular domains
c) Production of kinase domains whose activation loop cannot be phosphorylated
d) Production of kinase domains whose activation loop behaves as if always phosphorylated
e) Overexpression of the RTK
ADE
Dimerization is of crucial importance for the function of receptor tyrosine kinases because
In fact, it is not necessary for receptor tyrosine kinases to dimerize in order to be activated.
it increases the effective affinity of the receptors for ligand.
it protects the receptors from being phosphorylated and thereby desensitized.
it protects the receptors from being internalized and degraded.
it allows the receptor monomers to phosphorylate one another.
it allows the receptor monomers to phosphorylate one another.
SH2 domains specifically recognize:
phosphotyrosine residues in a specific amino acid sequence.
inverted repeats in DNA response elements.
proline rich sequences in target molecules.
phosphoserine residues in a specific amino acid sequence.
phosphothreonine residues in a specific amino acid sequence.
phosphotyrosine residues in a specific amino acid sequence.
What is the predicted phenotype for a population of cells with a mutation in Mad1 that dramatically increases Mad1’s affinity to kinetochores? In other words, the mutation causes Mad1 to stick tightly to kinetochores in all circumstances.
The cells become aneuploid
The cells progress rapidly through M-phase (the time to complete mitosis is reduced)
The anaphase-promoting complex is activated prematurely
The cells arrest in G2
The cells arrest in metaphase
The cells arrest in metaphase
Cyclin production serves as the timer for the cell cycle because…
Cells produce cyclin at a steady rate
Cyclin binds to cyclin-dependent kinase (CDK), thus activating it
The concentration of cyclin correlates with the activity level of CDK
An increased concentration of cyclin leads to an increased concentration of CDK
CDK phosphorylates molecules involved in cell cycle transitions
The concentration of cyclin correlates with the activity level of CDK
Suppose you discovered a drug that caused the immediate degradation of all cyclins in a cell. The drug degrades the cyclins only once, and the drug does not inhibit cyclin synthesis in any way. What would happen if you administered the drug in G2 phase?
CDK would become poly-ubiquitinated.
The cells would go through another round of DNA synthesis.
Nothing would happen.
The cells would enter and complete mitosis.
The cells would enter and arrest in mitosis.
The cells would go through another round of DNA synthesis.
Which of the following is a correct sequence of events for the metaphase-anaphase transition?
Closed-Mad2 binds to a Mad1/Mad2 tetramer, causing it to switch to Open-Mad2.
Mad1/Mad2 tetramers are released from unattached kinetochores, causing them to interact with p31.
Activated p31 binds to Closed-Mad2-Cdc20 complexes, releasing Cdc20.
Cdc20 binds the APC, the APC poly-ubiquitinates Separase
Securin cleaves cohesin molecules, allowing sister chromatids to separate.
Activated p31 binds to Closed-Mad2-Cdc20 complexes, releasing Cdc20.
Where is calcium stored by muscle cells?
Throughout the cytoplasm.
The Z-disk.
The A-disk.
The sarcoplasmic reticulum.
The myofibrils.
The sarcoplasmic reticulum.
Why are microtubules necessary for cell migration?
a) Because microtubules inhibit Rho
b) Because microtubules activate Rac
c) Because depolymerizing microtubules stops directed cell migration
d) Because microtubules create polarized zones of Rho and Rac
e) Because microtubules provide mechanical support to the lamellopodia
Because microtubules create polarized zones of Rho and Rac
Suppose you are able to engineer a mutant form of p31. This mutant p31 is hyper-active, “always on,” and 1000x more efficient than the wild-type. What would be a predicted phenotype of cells if you injected this mutant form into cells prior to anaphase?
Choose the best answer.
The cells would become aneuploid.
Nothing would happen.
Cyclin would be degraded prior to anaphase.
The cells would arrest in metaphase.
The mitotic spindle would collapse.
The cells would become aneuploid.
What is the GEF for ras?
Raf
MAPK
receptor with bound hormone
Sos
GRB2
Sos
All growth cones are:
Attracted to netrins and semaphorins
Repelled by netrins and semaphorins
Attracted to netrins and repelled by semaphorins
Repelled by netrins and attracted to semaphorins
None of the above.
None of the above.
