Exam 3 with answers - LAST NAME: __________________ FIRST...

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Unformatted text preview: LAST NAME: __________________ FIRST NAME: __________________ Exam #3 BIO 320 There are 30 multiple-choice questions worth 2 points each. Use a #2 pencil to answer the multiple-choice questions. WRITE AND MARK OFF THE BUBBLES FOR YOUR LAST NAME AND UT EID ON THE SCANTRON FORM There are 10 fill-in-the-blank questions, 2 points each. There are 3 essay questions worth a total of 20 points. Use a pen if you want a regrade for these questions. Write legibly and please do not ramble. Multiple choice questions, 2 points each 1) The affinity of the myosin II head for actin filament is greatest in which state? a. ATP-bound. b. ADP- and Pi- bound. c. ADP bound (with Pi released). d. Not bound to any nucleotide. e. Both b and c there is no difference between the two. 2) Which of the conditions listed below will decrease the likelihood of skeletal muscle contraction? a. Addition of a drug that blocks Ca2+ binding to troponin. b. An increase in the amount of ATP in the cell. c. A mutation in tropomyosin that decreases its affinity for the actin filament. d. A mutation in the sarcoplasmic reticulum Ca2+-releasing channel that increases its efficiency. e. None of the above. 3) Which of the following is true of skeletal muscle contraction? a. Actin filaments shrink in length during contraction while myosin filaments retain their starting length. b. Actin filaments retain their starting length while myosin filament shrink in length during contraction. c. Both actin and myosin filaments retain their starting length. d. Z discs remain stationary relative to each other during contraction. e. The elastic protein titin retain its starting length. 4) Which of the statements below about intermediate filaments is INCORRECT? a. They can be found in the cytoplasm and the nucleus. b. They can be anchored to the plasma membrane. c. They do not undergo dynamic instability. d. Once assembled, they all do not undergo rearrangements. e. They generally can withstand relatively large shear forces. 5) M-Cdk is activated by: a. Phosphorylation by Wee1. b. Dephosphorylation by Wee1. c. Phosphorylation by Cdc25 d. Dephosphorylation by Cdc25. e. Both a and c. 6) Which of the following is not a result of M-Cdk activation? a. Degradation of CAK. b. Phosphorylation of the M-cyclin subunit. c. Activation of APC/C. d. Poly-ubiquitination of M-cyclin. e. Both c and d. 7) A mutant yeast strain stops proliferating when shifted from 25C to 37C. When these cells are analyzed at the two different temperatures, using a machine that sorts cells according to the amount of DNA they contain, the graphs on the right are obtained. Which of the following would NOT explain the results with the mutant? a. inability to initiate DNA replication. b. inability to begin M phase. c. inability to activate proteins needed to enter S phase. d. inappropriate production of a signal that causes the cells to remain in G1. e. none of the above. 25oC number of cells 1 2 amount of DNA/cell (arbitrary units) 37oC number of cells 1 2 amount of DNA/cell (arbitrary units) 8) Which of the following signaling molecules acts to relax smooth muscle? a. Thyroxine. b. Cortisol. c. Morphogen. d. Nitric oxide. e. Acetylcholine. 9) Which of the following is NOT a way to control the activity of Cdk complexes? a. Cyclin and CKI synthesis. b. Cdk dephosphorylation. c. Cdk phosphorylation. d. Cdk degration. e. Cyclin and CKI degradation. 10) What would be the most obvious outcome of repeated cell cycles consisting of S phase and M phase only? a. Cells would not be able to condense their chromosomes. The mitotic spindle could not assemble. Cells would get larger and larger. The cells produced would get smaller and smaller. Cells would not be able to undergo cytokinesis. 11) In response to DNA damage, G1 cells remain in G1 partly because? a. The p21 CKI is degraded. b. Cdc25 is retained in the cytoplasm. c. Mdm2 becomes phosphorylated. d. p53 is exported from the nucleus. e. APC is activated. The correct answer should be none of the above. All students will get 2 points. 12) S-Cdk triggers entry into S phase by phosphorylating and? a. activating Cdc6. b. inactivating ORC. c. activating a number of replication enzymes. d. activating Rb. e. inactivating G1/S-cyclin. 13) Which of the following statements is INCORRECT? a. Astral microtubules play a role in centrosome separation. b. Interpolar microtubules play a role in chromosome alignment during congression. c. Kinetochore microtubules are important for spindle elongation during anaphase B. d. Astral microtubules can help to position the site of cytokinesis. e. Each human kinetochore can attach to multiple microtubules. 14) Unattached kinetochores inhibit the onset of anaphase by activating a checkpoint protein called: a. Separase. b. Mad2. c. Cohesin. d. Cdc20. e. Polo kinase 15) Which of the following statements about the anaphase-promoting complex (APC) is INCORRECT? a. It promotes the degradation of proteins that regulate M phase. b. It causes decrease in M-Cdk activity. c. It promotes the degradation of separase. d. M-Cdk stimulates its activity. e. It functions as an E3. b. c. d. e. 16) Chromosomes condense only during M phase because? a. condensin is made only during M phase. b. M-Cdk phosphorylates and activates condensin. c. condensin has access to chromosomes only after nuclear envelope breakdown. d. condensin is activated by APC. e. a and b. 17) For the following modes of cell signaling, the distance in which the signaling molecule has to travel the LARGEST DISTANCE is in the order of: a. paracrine > endocrine > synaptic > contact-dependent. b. endocrine > synaptic > paracrine > contact-dependent. c. contact-dependent > paracrine > synaptic > endocrine. d. synaptic > paracrine > contact-dependent > endocrine. e. endocrine > paracrine > synaptic > contact-dependent. 18) The primary function of cAMP in most eukaryotic cells is to activate: a. G. b. protein kinase A. c. MAP kinase. d. phospholipase C. e. glycogen synthase. 19) Phospholipase C produces which of the following second messengers? a. PI(4,5)P2 and PI(3,4,5)P3. b. Calcium and cGMP. c. Diacylglycerol and phosphatidylinositol. d. Diacylglycerol and IP3. e. cAMP and calcium. 20) Most mitogens act through which signaling pathway to promote cell proliferation? a. Ras/MAP kinase. b. Adenylyl cylcase/cAMP. c. cGMP/phosphodiesterase. d. DAG/IP3. e. Calcium/calmodulin. 21) The following happens when a cell-surface receptor activates a trimeric G protein. a. The subunit exchanges its bound GDP for GTP. b. The GDP bound to the subunit is phosphorylated to form bound GTP. c. The subunit exchanges its bound GDP for GTP. d. It activates the subunit and inactivates the complex. e. The trimeric G protein becomes tightly associated with the receptor. 22) 23) 24) 25) Protein kinase C is activated by direct binding to: a. calcium and calmodulin. b. calcium and IP3. c. calcium and diacylglycerol. d. calcium alone. e. diacylglycerol and IP3. In vertebrate vision, the second messenger regulating gated ion channels is? a. cAMP. b. PKA. c. cGMP. d. DAG. e. IP3. Which of the following mechanisms is NOT directly involved in inactivating an activated receptor tyrosine kinase? a. Synthesis and activation of an RGS protein. b. Dephosphorylation by protein tyrosine phosphatases. c. Removal of the receptor from the plasma membrane by endocytosis. d. Degradation of the receptor in lysosomes. e. All of the above are directly involved. Which type of junction involves a connection to the actin cytoskeleton? a. Adherens junctions. b. Desmosomes. c. Tight junctions. d. Gap junctions. e. Synaptic junctions. 26) Which type of cell-cell adhesion protein involves association with oligosaccharides? a. Cadherin. b. Immunoglobulin superfamily protein. c. Integrin. d. Selectin. e. ICAM. 27) Which type of junction contributes the most to the polarization of epithelial cells? a. Adherens junctions. b. Desmosomes. c. Tight junctions. d. Gap junctions. e. Synaptic junctions. 28) Which of the following cell-cell adhesion proteins function EXCLUSIVELY through homophilic interactions? a. Cadherin. b. Selectin. c. Immunoglobulin superfamily protein. d. Integrin. e. None of the above. 29) Congression during mitosis DOES NOT involve? a. Depolymerization of microtubules at leading kinetochore. b. Minus end-directed motor at leading kinetochore. c. Polymerization of microtubules at lagging kinetochore. d. Plus end-directed motor at lagging kinetochore. e. All of the above are involved. 30) Shown on the right is the electron micrograph image of a cross section of a muscle cell. The structure highlighted by the arrow contains: a. Actin filament. b. Myosin filament. c. Nebulin. d. Titin. e. Myofibril. Fill in the blank with one or a small number of appropriate words, 2 points each. 1. G-protein-coupled receptors (GPCRs) all have a similar structure with _______seven___________ transmembrane domains. 2. _____Gap junctions____ allow neighboring cells to communicate through the diffusion of intracellular small molecules. 3. The abundance of a given cyclin ____fluctuates/varies____ through the cell cycle whereas, in most cases, the abundance of cyclin-dependent kinases ____stays constant____. 4. Phosphorylation of ______Rb_______ by G1-Cdk allows the transcription factor E2F to initiate the events that lead to G1 to S transition. 5. ___Aurora-B kinase___ causes the detachment of microtubules from kinetochores that are not under sufficient tension. 6. The signal for endocytosis and lysosomal destruction of receptor tyrosine kinases is __mono- ubiquitination_______________. 7. Microtubules are ____more dynamic____________________________ during M phase (to facilitate kinetochore-microtubule attachment). 8. p53 is often inactivated mutationally in _______cancer_________ cells. 9. Spindle elongation during anaphase B involves a _____minus_________ end-directed motor at the cell cortex and a ___plus____________end-directed motor at the interdigitating interpolar microtubules. 10. It is possible for many myosin II molecules to function together during skeletal muscle contraction without interfering with each other because each myosin II molecule is a ____non- processive_____________________________ motor. Assay questions. 1. Antibodies are Y-shaped molecules that have two identical binding sites. When antibodies for a particular receptor tyrosine kinase are added to cells, they often cause activation of this kinase. In contrast, addition of antibodies for GPCRs generally does not activate such GPCRs. Explain why this difference. (6 points) Antibodies to RTK bring 2 RTKs together (induced proximity), allowing the (weak) kinase activity of each to trans-phosphorylate the other, leading to full activation of the kinase activity of each RTK. Activation of GPCRs does NOT involve induced proximity of 2 GPCR molecules. (Instead, GPCR becomes a GEF for G) 2. In terms of cell cycle progression, what would happen to a mutant cell that synthesizes a form of M-cyclin that cannot be phosphorylated by M-Cdk? Explain your answer. (6 points) Without phosphorylation by M-Cdk, M-cyclin is NOT (poly-)ubiquitinated by APC/C. Thus, M-cyclin will not be degraded (in the proteasome). As a result, M-Cdk activity remains high, and mutant cell will remain in M phase (i.e., no entry into G1) 3. Sister chromatids are not held together in cells that do not make cohesin. After these cells enter M phase, activation of the anaphase-promoting complex (APC) is delayed when compared to the situation in wild-type cells. What happens to the stability of kinetochore-microtubule attachment in these mutant cells relative to the situation in wild-type cells? Explain your answer. (4 points) When sister chromatids are not held together, the force that pulls on (sister) kinetochores is not opposed. Hence, there is no tension on kinetochores. Aurora-B kinase will cause detachment of microtubules from such kinetochores. Thus, kinetochore-microtubule attachment will be unstable. Briefly explain why activation of anaphase-promoting complex (APC) is delayed in these mutant cells. (4 points) Unattached kinetochores activate the spindle assembly checkpoint (SAC). Mad2 (and other checkpoint proteins) becomes activated at unattached kinetochores. Activated Mad2 (and other checkpoint proteins) binds to and inhibits APC, leading to delay in APC activation. ...
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This note was uploaded on 02/06/2012 for the course BIO 320 taught by Professor Staff during the Spring '08 term at University of Texas at Austin.

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