BIOL2S:3Eam 4atzCOpage ae, BIOL2533 Cell Biology Fall 2008 __EXAM4 [ MULTIPLE CHOICE. Choose the one alternative that best completes the stat question. Circle the answer on the exam and mark the appropriate box on t | Please pput your name and ID# on the Scantron answer sheet. Remembs Scantronare the final answers | accept. Each question worth 2.8 poin Scantron answer sheet. the answers you give on the jent or answers the ] = Generates two second messenger molecules diacylglycerol and phosphotiylinositol phosphates (PIP3) when activated. 2] Phospholipase C d. adenylate cyclase < B. G-coupled protein receptors e. Ras ©. Phospholipase B v2. DNA replication occurs during what part of the celll cycle? A a. G, phase d. Mphase ae [7B] S phase ©. Go phase ©. Gyphase 3 The human papillomavirus E6 and E7 genes exemplify which of the following. 2, tumor suppressor genes 4d, growth inhibitory factors b. CDK inhibitors cyclin-dependent kinases &., oncogenes 74, What is the mechanism by which Caks g a. association with steroid hormones b. proteolytic cleavage ¢. binding to a transcription factor et activated during various phases of the cell cycle? .. association with the appropriate cyclin ©. Cdk binding a cell-surface growth factor t - rotein kinase A (PKA) is activated by: @. phosphorylation of the catalytic domain by RAS . binding of phosphotidy!-inositol phosphate to its regulatory domain ©. phosphorylation of its regulatory domain by RAS re g, binding of cAMP to its regulatory domain “€. binding of cAMP to its catalytic domain Moss what mechanism does pRb prevent cells from enteri : a. pRb binds directly to specific sites on the genome, act phase transition. b PRb proteolytically degrades members of the E2F transcription family that are required for § hase activities. E fone prevents E2F transcr v ing S phase of the cell cyclg?~ tivating specific genes that prevent $ ition factors from binding to specific S phase genes and activating jem, d. PRD activates E2F transcription factors causing them to bind to Specific S phase genes and activating them, @. none of the above‘BLOL2S35/Exam 4F 2008/page 2 NAME: oe 71 The period in the cell cycle between the end of DNA replication and the beginning of mitosis is called the phase Gy dM ms TE,‘none of the above c. Gy “ las “56. What happens immediately after most receptor Protein-tyrosine kinases bind to thei ligand? ‘a. receptor trimerization d. receptor dissociation ‘BI receptor dimerization deppegr® €. candd ‘T. receptor denaturation 9 The class of enzymes involved in triggering the various stages of the cell cycle are called @. proteases d phosphatases b. transferases € methylases {kinases “10. With regard to hormone signaling, the release of a hormone from cells to signal nearby cells in tthe same organ would be referred to as_ Pas. rjne-_ signaling a. autocrine 4. exocrini - 7B. paracrine ©. either bore @ endocrine “11. The alpha suburit of a heterotrimeric G protein is active when bound to: a. the beta and gamma subunits d, GDP b. the G-coupled protein receptor [ejcte ©. phosphorylated tyrosines on receptor tyrosine kinases \¥2. The alpha subunit of G protein is responsible for activation of to produce ‘a. Ras; diacylgylcerol [Gjadenylate cyciase, cAMP b. Phospholipase C; cAMP. ‘. none of the above ©. G-coupled protein receptors; diacylglycerol PEP eccivias are cancers that originate in epithelial cells and comprise the majority ofall cancers a. Sarcomas d. Leukemias b. Lymphomas @. none of the above / TEjCarcinomas “44. Where are steroid receptors generally located and where do they bind the steroid hormone once it enters the cell? Ta] They are located and bind the steroids in the cytoplasm B. They are located and bind the steroids in the middle of the cell membrane. ¢ They are located and bind the steroids on the extracellular membrane surface. d. They are located and bind the steroids on the intracellular membrane surface © The receptors are located in the cytoplasm but they bind their ligands in the lysosomesBIOL25)¥xam aFaiz008/page 3 Peis LD, “AS Damage to DNA that takes place during DNA replication results in the arrest of normal cells at the J oe lun G2tom y Sr G1-40-S %. Mto-G1 > é ic. S-to-G1 46. Which cell surface receptors conduct a flow of ions across the plasma membrane when bound to igand? 1B} ligand-gated channels 4. steroid hormone receptors BRTKS. e. GPCRs EE G protein coupled receptors here is the guanine nucleotide (GTP/GDP) -binding site of the G protein located? ‘on the G,subunit . on the Gsysubunit . on the Gysubunt e. none of the above . on the G,subunit “48 How do mutations of the RAS gene lead to tumor formation? They cause premature hydralysis of the Res proten’s bound GTP. ‘They cause the rapid denaturation of the ea protein They prevent the hr olyis ofthe Ras proters bound GTP. The mutant version ofthe Ras protein stays turned on and cannot be regulated add ms i. enzyme does diacylglycerol (DAG) recruit and activate? { phosphatidylinositol (PI)-specific phospholipase C-y 4. glycogen phosphorylase — kinase A . phosphorylase kinase protein kinase C __ 20. Which ofthe folowing activites helps to amply the signal generate fom the agin hormone artivng atthe call surtace and nding to is ceptor? Each PKA calaiyicsubunt phosphoryates a large number of phosphorjase Kinases b. Each adenyiy eyclase molecule produces many cAMP melecules whens aclvated ¢. Each phosphoryiase catalyzes, n un, the formation of much larger narber of ucose phosphate: 4, Each cAMP bande to one hormone receptor nthe plese membrane abande How is Ras activity tured off? 12, Wisturned ofl phoephoryation | TE. turned off by hyaro}ysis of ts bound GTP to GOP. © iis turned offby hydrolysis of ts bound GDP to GTP | lis turned off by an aloterieinhibtor \ ® ilistumed off by hydroysie of ts bound GTP to GMP. "22. Cells that have stopped dividing and are arrested in a stage preceding the DNA synthesis are. id tobe ina___state. a. G, phase _d. Mphase b Sphase Gy phase © G, phaseB1OL2533/Exam 4/Fal12008/page 4 NAME:, LD. 23. According to the original proposal of cell cycle checkpoints, what circumstances lead to a halt intr y progress of the cell cycle? / @. when any of the chromosomal DNA is damaged ~~ J b. when mitochondrial DNA is damaged when certain critical processes have not been properly completed, lite DNA replication durins 'S phase or chromosome alignment during M phase . d. when the lysosomes get too big aandc 4: How do the nuclei of normal cells differ from the nuclei of cancer cells? a. Cancer cell nuclei are invariably smaller than those of normal cells b. Cancer cell nuclei are invariably larger than those of normal cells. ¢_ Cancer cells often exhibit more frequent apoptosis than normal cells [Cancer cells often have highly aberrant chromosome complement none of the above Why do tumor viruses transform normal cells into cancer celis? ; ~a,, They take over the normal cells and cause them to make progeny viruses. X x Bd. They carry genes whose products interfere with the cell's normal growth-regulating activities, \~ 7 © They carry genes whose products interfere with the cell's normal bioenergetics pathways 4. They carry genes whose products interfere with the calls normal secretory activities. e.a,candd , ‘Oncogenes 4. encode proteins that promote the loss of growth control < wb. encode proteins that promote the conversion of a cell to the malignant state Ae, May act as accelerators of cell proliferation and tumorigenesis Bjsearae encode proteins that restrain cell growth and prevent malignancy *, } ich.a.the. following statements is.a.valid- explanation for the relative rarity of cancer? ! Cancer development requires more than one genetic alteration | Cancer development is a one-step process characterized by a progression of permanent alterations in a single cell line, & Cancer development is a multistep process characterized by a progression of permanent alterations in multiple independent cells at the same time -& Each change makes the cell less responsive to the body's regulatory machinery. ©. aandd f 6. What enzyme is responsible for maintaining the length of the DNA sequences on the ends of chromosomes (telomeres)? a. tendrilase d. telomere disruptase TB] telomerase e. telomere kinase | , ©. telomere synthase / { 9. Suwor-auppressor genes , U encode proteins that resirain call growth \/ b. encode proteins that prevent malignancy © encode proteins that enhance cell growth and division rates oG_-encode proteins that keep the cell cycle running ‘el aandbBIOL253/Exam 4/Falt2008/page 5 NAME Resi Stee ape iaripiw at ot aabecarh pe. Inygeneral, the development of a malignant tumor requires J alterations in tumor-suppressor genes.” 4d. a full oncogene complement » i+": alterations in oncogenes? e. aandb 7 ©. a full tumor-suppressor gene complement part of the cell cycle does the pRb protein help to regulate? ‘3 ~ Str d. the Go~ G, transition 2. the MG transition 9 sat i & the G2 - M transition Aa wiv knowing anything about activation of progestrone production, use your knowledge of FICRs to predict the sequence of events leading to the production of progestrone in normal? (LH is the ligand binding the GPCR). 1— CAMP production begins. 2 ~The G protein activates adenylyl cyclase. 3 The LH receptor activates its G protein. 4~ Testosterone production is triggered 6 — LH binds to LH receptors on testicular cell ‘surfaces. 5-3-2-4-4 4f 3-5-2-1-4 5-3-2-1-4 e 5-3-1-2-4 eo 5-2-3-1-4 et are surveillance mechanisms that halt the progress of the cell cycle if any of the various events that make up the cell cycle are not working correctly or are not happening in the correct order watchers d. surveillosomes T checkpoints €. monitorosomes © checkups 34: What is the most important property of a cancer cell, whether itis in the body or the culture dish? a. its chromosome complement 4. its secretions 2b] its loss of growth control €. its inability to divide ¢ its size 35. Human papillomavirus causes cancer by 2. inactivation of R's abily to inhibit E2F function,» », inactivation of p53's abilly to inhibit E2F function €. inactivation of p§3's abiity to initiation apotosis, »— ¢. both a and b ©] both a and c | order to be highly active, a Cdk-cyclin needs to be Ei] phosphorylated d. bound by cAMP br methylated ©. cleaved by a protease ©. acetylated “37, Genes that cause cancer due to their ‘overexpression are called: falyoncogenes 4. tumor promoter genes BY tumor suppressor genes @. none of the above © proto-cancer genes1.2553/Exam A/F H12008/page 6 LD. 46. You have recently identified a molecule that you believe to be a ligand associated with a signal transduction mechanism. All you know about this ligand is that chemically itis hydrophilic. As a result, you expect it to interact with its receptor: fe ‘AJ at the outer cell surface e > within the cytoplasm of the cel! . within the nucleus of the cell 4. on the cytoplasmic side of the plasma membrane e. any on the above are possible Place the following steps in the MAP kinase cascade in the proper order. —MAPKKK is phosphorylated + 2- MAPKK phosphorylates and activates a MAP kinase. ~The phosphorylated tyrosine residues of the receptor are bound by the Grb2-Sos complex formec inthe cytoplasm, recruiting it tothe inner surface of the plasma membrane, close to Ras — 4— Phosphorylated MAPKKK, phosphorylates the MAPKK. ~-5 ~ Ras binds to MAPKKK, a signaling protein ~~ Sos causes Ras to exchange GDP for GTP, activating it. 7 —MAP kinase moves into the nucleus where it phosphorylates and activates specific transcription factors. 4 Aligand binds to its receptor activating the receptor. A 8-5-3-6-1-4-2-7 #8-3-6-4-5-2-1-7 b. 8-3-6-5-7-2-4-1 2 8-3-7-5-4-1-2-6 J8-3-6-5-1-4-2-7 “40. Which of the following is a second messenger {hat has been found in eukaryotic cells? Ya, diacylglycerol d. inositol triphosphates b. cyclic AMP £8] all of the above . nitric oxide