BIOS2114 EXAM 4 MULTIPLE CHOICE

(c) G2

A mutant yeast strain stops proliferating when shifted from 25°C to 37°C. 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 below are obtained. At which stage in the cell cycle is this mutant arrested? (a) G1 (b) S (c) G2 (d) M

(d) interact with signal molecules that diffuse through the plasma membrane

All members of the steroid hormone receptor family _______________________ (a) are cell-surface receptors (b) do not undergo conformational changes (c) are found only in the in the cytoplasm (d) interact with signal molecules that diffuse through the plasma membrane

(c) cohesins

At the end of DNA replication, the sister chromatids are held together by the ___________________ (a) kinetochores (b) securins (c) cohesins (d) histones

(b) oncogenes

Genes that encode growth factor receptors that when mutated no longer require the growth factor to activate cell division would be termed ____________________ (a) proto-oncogenes (b) oncogenes (c) tumor suppressors (d) unregulated cell division (e) regulated cell division

(d) at the end of G2

In which phase of the cell cycle do cells check to determine whether the DNA is fully and correctly replicated? (a) at the transition between G1 and S (b) when cells enter G0 (c) during M (d) at the end of G2

(d) cyclin levels change during the cycle

Levels of Cdk activity change during the cell cycle, in part because (a) the Cdks phosphorylate each other (b) the Cdks activate the cyclins (c) Cdk degradation precedes entry into the next phase of the cell cycle (d) cyclin levels change during the cycle

(a) proto-oncogenes

Proteins that function as a receptor that normally turns on cell division in response to a growth factor would be termed ______________________ (a) proto-oncogenes (b) oncogenes (c) tumor suppressors (d) unregulated cell division (e) regulated cell division

(c) tumor suppressors

Proteins that normally function to inhibit cell division would be termed _________________________________________ (a) proto-oncogenes (b) oncogenes (c) tumor suppressors (d) unregulated cell division (e) regulated cell division

(c) a proto-oncogene

Ras is a GTP-binding protein that is often defective in cancer cells. A common mutation found in cancer cells causes Ras to behave as thought it were bound to GTP all the time, which will cause cell to divide inappropriately. From this description, the normal Ras gene is _________________ (a) a tumor suppressor (b) an oncogene (c) a proto-oncogene (d) a gain-of-function mutation

(c) the α subunit exchanged its bound GDP for GTP

The following happens when a G-protein-coupled receptor activvates a G protein (a) the β subunit exhcnages its bound GDP for GTP (b) the GDP bound to the α subunit is phosphorylated to form bound GTP (c) the α subunit exchanged its bound GDP for GTP (d) it activates the α subunit and inactivates the βγ

(b) a mutation that prevents RGFR from binding to RGF

The growth factor RGF stimulates proliferation of cultured rat cells. The receptor that binds RGF is a receptor tyrosine kinase called RGFR. Which of the following types of alteration to RGF would be most likely to prevent receptor dimerization? (a) a mutation that increases the affinity of RGFR for RGF (b) a mutation that prevents RGFR from binding to RGF (c) changing the tyrosines that are normally phosphorylated on RGFR dimerization to alanines (d) changing the tyrosines that are normally phosphorylated on RGFR dimerization to glutamic acid

(c) a mutation that inactivates the protein tyrosine phosphatase that normally removes the phosphates from tyrosines on the activated receptor

The growth factor Superchick stimulates the proliferation of cultured chicken cells. The receptor that binds Superchick is a receptor tyrosine kinase (RTK), and many chicken tumor cell lines have mutations in the gene that encodes this receptor. Which of the following types of mutation would be expected to promote uncontrolled cell proliferation? (a) a mutation that prevents dimerization of the receptor (b) a mutation that destroys the kinase activity of the receptor (c) a mutation that inactivates the protein tyrosine phosphatase that normally removes the phosphates from tyrosines on the activated receptor (d) a mutation that prevents the binding of the normal extracellular signal to the receptor

(a) addition of a drug that causes cyclic AMP phosphodiesterase to be hyperactive

You are interested in cell-size regulation and discover that signaling through a GPCR called ERC1 is important in controlling cell size in embryonic rat cells. The G protein downstream of ERC1 activates adenylyl cyclase, which ultimately leads to the activation of PKA. You discover that cells that lack ERC1 are 15% smaller than normal cells, while cells that express a mutant, constitutively activated version of PKA are 15% larger than normal cells. Given these results, which of the following treatments to embryonic rat cells should lead to smaller cells? (a) addition of a drug that causes cyclic AMP phosphodiesterase to be hyperactive (b) addition of a drug that prevents GTP hydrolysis by Gα (c) addition of a drug that activates adenylyl cyclase (d) addition of a drug that mimics the ligand of ERC1

(d) unregulated cell division

The transition of a proto-oncogene to an oncogene leads to ________________________ (a) proto-oncogenes (b) oncogenes (c) tumor suppressors (d) unregulated cell division (e) regulated cell division

(b) M-Cdk

What does Cdc25 regulate? (a) S-Cdk (b) M-Cdk (c) APC complex (d) M cyclin (e) S cyclin

(c) phosphatase

What is the enzymatic activity of *Cdc25*? (a) cyclin binding (b) ubiquitin-mediated proteolysis (c) phosphatase (d) kinase

(d) kinase

What is the enzymatic activity of *M-cdk*? (a) cyclin binding (b) ubiquitin-mediated proteolysis (c) phosphatase (d) kinase

(a) Initiating the exchange of bound GDP for GTP.

What is the mechanism of transduction for a G protein-coupled receptor? (a) Initiating the exchange of bound GDP for GTP. (b) Cleavage of a bound GTP to GDP. (c) Phosphorylation of receptor dimers on the intracellular side. (d) Removal of a covalently attached phosphate group from a protein. (e) Gating of an ion channel.

(c) Phosphorylation of receptor dimers on the intracellular side.

What is the mechanism of transduction for a receptor tyrosine kinase? (a) Initiating the exchange of bound GDP for GTP. (b) Cleavage of a bound GTP to GDP. (c) Phosphorylation of receptor dimers on the intracellular side. (d) Removal of a covalently attached phosphate group from a protein. (e) Gating of an ion channel.

(b) BRCA1

Which of the following genes function in DNA repair? (a) Ras (b) BRCA1 (c) Myc (d) Rb (e) Cdc25

(a) a mutation that introduces a stop codon immediately after the codon for the initiator methionine

Which of the following genetic changes cannot convert a proto-oncogene into an oncogene? (a) a mutation that introduces a stop codon immediately after the codon for the initiator methionine (b) a mutation within the coding sequence that makes the protein hyperactive (c) an amplification of the number of copies of the proto-oncogene, causing overproduction of the normal protein (d) a mutation in the promoter of the proto-oncogene, causing the normal protein to be transcribed and translated at an abnormally high level

(c) adenylyl cyclase

Which of the following is the activating enzyme for a cascade that uses cAMP as a second messenger? (a) kinase (b) phosphatase (c) adenylyl cyclase (d) phosphodiesterase

(c) a mutation in even a single cancer-critical gene is sufficient to convert a normal cell into a cancer cell

Which of the following statements about cancer is *false*? (a) viruses cause some cancers (b) tobacco use is responsible for more than 20% of all cancer deaths (c) a mutation in even a single cancer-critical gene is sufficient to convert a normal cell into a cancer cell (d) chemical carcinogens cause cancer by changing the nucleotide sequence of DNA

(d) metaphase to anaphase

Which of the following transitions in the cell cycle is not controlled by a cyclin-dependent kinase? (a) G1 restriction point (b) G1 to S (c) G2 to M (d) metaphase to anaphase (e) none of the above: they are all controlled by a cyclin-dependent kinase

B

Which of the peaks in the graph at right would be cells in G2?