Bil 255 Final Exam

Adrenaline stimulates glycogen breakdown in skeletal muscle cells by ultimately activating glycogen phosphorylase, the enzyme that breaks down glycogen, as shown in the figure. Which of the following statements is false? (a) A constitutively active mutant form of PKA in skeletal muscle cells would lead to a decrease in the amount of unphosphorylated phosphorylase kinase. (b) A constitutively active mutant form of PKA in skeletal muscle cells would not increase the affinity of adrenaline for the adrenergic receptor. (c) A constitutively active mutant form of PKA in skeletal muscle cells would lead to an excess in the amount of glucose available. (d) A constitutively active mutant form of PKA in skeletal muscle cells would lead to an excess in the amount of glycogen available.

A constitutively active mutant form of PKA in skeletal muscle cells would lead to an excess in the amount of glycogen available.

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.

A mutation that introduces a stop codon immediately after the codon for the initiator methionine.

After isolating the rough endoplasm reticulum from the rest of the cytoplasm, you purify the RNA's attached to it. Which of the following proteins do you expect the RNA from the rough endoplasmic reticulum to encode? (a) soluble secreted proteins (c) plasma membrane proteins (b) ER membrane proteins (d) all of the above

All of the above

The figure shows that intracellular signaling pathways can be highly interconnected. From this information, which of the following statements is incorrect? (a) The GPCR and the RTK both activate phospholipase C. (b) Activation of either the GPCR or the RTK will lead to activation of transcriptional regulators. (c) CaM-kinase is only activated when the GPCR is active and not when the RTK is active. (d) Ras is activated only when the RTK is active and not when the GPCR is active.

CaM-kinase is only activated when the GPCR is active and not when the RTK is active.

Akt promotes the survival of many cells by affecting the activity of Bad and Bcl2, as diagrammed in the figure. Which of the following statements is false? (a) In the presence of a survival signal, Akt is phosphorylated. (b) In the absence of a survival signal, Bad inhibits the cell-death inhibitor protein Bcl2. (c) In the presence of a survival signal, the cell-death inhibitory protein Bcl2 is active. (d) In the absence of a survival signal, Bad is phosphorylated.

In the absence of a survival signal, Bad is phosphorylated.

What is the role of the nuclear localization sequence in a nuclear protein? (a) It is bound by cytoplasmic proteins that direct the nuclear protein to the nuclear pore. (b) It is a hydrophobic sequence that enables the protein to enter the nuclear membranes. (c) It aids in protein unfolding so that the protein can thread through nuclear pores.(d) It prevents the protein from diffusing out of the nucleus through nuclear pores.

It is bound by cytoplasmic proteins that direct the nuclear protein to the nuclear pore

How does S-Cdk help guarantee that replication occurs only once during each cell cycle? (a) It blocks the rise of Cdc6 concentrations early in G1. (b) It phosphorylates and inactivates DNA helicase. (c) It phosphorylates the Cdc6 protein, marking it for destruction. (d) It promotes the assembly of a prereplicative complex.

It phosphorylates the Cdc6 protein, marking it for destruction.

The lab you work in has discovered a previously unidentified extracellular signal molecule called QGF, a 75,000-dalton protein. You add purified QGF to different types of cells to determine its effect on these cells. When you add QGF to heart muscle cells, you observe an increase in cell contraction. When you add it to fibroblasts, they undergo cell division. When you add it to nerve cells, they die. When you add it to glial cells, you do not see any effect on cell division or survival. Given these observations, which of the following statements is most likely to be true? (a) Because it acts on so many diverse cell types, QGF probably diffuses across the plasma membrane into the cytoplasm of these cells. (b) Glial cells do not have a receptor for QGF. (c) QGF activates different intracellular signaling pathways in heart muscle cells, fibroblasts, and nerve cells to produce the different responses observed. (d) Heart muscle cells, fibroblasts, and nerve cells must all have the same receptor for QGF.

QGF activates different intracellular signaling pathways in heart muscle cells, fibroblasts, and nerve cells to produce the different responses observed.

The figure shows the orientation of the Krt1 protein on the membrane of a Golgi-derived vesicle that will fuse with the plasma membrane. Given this diagram, which of the following statements is true? (a) When this vesicle fuses with the plasma membrane, the entire Krt1 protein will be secreted into the extracellular space. (b) When this vesicle fuses with the plasma membrane, the C-terminus of Krt1 will be inserted into the plasma membrane. (c) When this vesicle fuses with the plasma membrane, the N-terminus of Krt1 will be in the extracellular space. (d) When this vesicle fuses with the plasma membrane, the N-terminus of Krt1 will be cytoplasmic.

When this vesicle fuses with the plasma membrane, the N-terminus of Krt1 will be in the extracellular space

The figure shows the pathway through which nitric oxide (NO) triggers smooth muscle relaxation in a blood-vessel wall. Which of the following situations would lead to relaxation of the smooth muscle cells in the absence of acetylcholine? (a) a smooth muscle cell that has a defect in guanylyl cyclase such that it cannot bind NO (b) a muscle cell that has a defect in guanylylcyclase such that it constitutively converts GTP to cyclic GMP (c) a muscle cell that has cyclic GMP phosphodiesterase constitutively active (d) a drug that blocks an enzyme involved in the metabolic pathway from arginine to NO

a muscle cell that has a defect in guanylylcyclase such that it constitutively converts GTP to cyclic GMP

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 though it were bound to GTP all the time, which will cause cells to divide inappropriately. From this description, the normal Ras gene is (a) a tumor suppressor. (c) a proto-oncogene. (b) an oncogene. (d) a gain-of-function mutation.

a proto-oncogene.

Acetylcholine binds to a GPCR on heart muscle, making the heart beat more slowly. The activated receptor stimulates a G protein, which opens a K+ channel in the plasma membrane, as shown in the figure. Which of the following would enhance this effect of (a) addition of a high concentration of a nonhydrolyzable analog of GTP (b) addition of a drug that prevents the α subunit from exchanging GDP for GTP (c) mutations in the acetylcholine receptor that weaken the interaction between the receptor and acetylcholine (d) mutations in the acetylcholine receptor that weaken the interaction between the receptor and the G protein

addition of a high concentration of a nonhydrolyzable analog of GTP

Apoptosis differs from necrosis in that necrosis (a) requires the reception of an extracellular signal. (b) causes DNA to fragment. (c) causes cells to swell and burst, whereas apoptotic cells shrink and condense. (d) involves a caspase cascade.

causes cells to swell and burst, whereas apoptotic cells shrink and condense.

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.

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.

cyclin levels change during the cycle.

Single Sequences that direct proteins to the correct compartment are (a) added to proteins through post-translational modification. (b) added to a protein by a protein translocator. (c) encoded in the amino acid sequence and sufficient for targeting a protein to its correct destination. (d) always removed once a protein is at the correct destination.

encoded in the amino acid sequence and sufficient for targeting a protein to its correct destination

You have isolated a strain of mutant yeast cells that divides normally at 30°C but cannot enter M phase at 37°C. You have isolated its mitotic cyclin and mitotic Cdk and find that both proteins are produced and can form a normal M-Cdk complex at both temperatures. Which of the following temperature-sensitive mutations could not be responsible for the behavior of this strain of yeast? (a) inactivation of a protein kinase that acts on the mitotic Cdk kinase (b) inactivation of an enzyme that ubiquitylates M cyclin (c) inactivation of a phosphatase that acts on the mitotic Cdk kinase (d) a decrease in the levels of a transcriptional regulator required for producing sufficient amounts of M cyclin

inactivation of an enzyme that ubiquitylates M cyclin

The Retinoblastoma (Rb) protein blocks cells from entering the cell cycle by _________________. (a) phosphorylating Cdk. (c) inhibiting cyclin transcription. (b) marking cyclins for destruction by proteolysis. (d) activating apoptosis.

inhibiting cyclin transcription

Different glycoproteins can have a diverse array of ogliosaccharides. Which of the statements below about this diversity is true? (a) Extensive modification of oligosaccharides occurs in the extracellular space. (b) Different oligosaccharides are covalently linked to proteins in the ER and the Golgi. (c) A diversity of oligosaccharyl transferases recognizes specific protein sequences, resulting in the linkage of a variety of oligosaccharides to proteins. (d) Oligosaccharide diversity comes from modifications that occur in the ER and the Golgi of the 14-sugar oligosaccharide added to the protein in the ER.

ogliosaccharide diversity comes from modifications that occur in the ER and the Golgi of the 14-sugar ogliosaccharide added to the proteins in the ER

The length of time a G protein will signal is determined by (a) the activity of phosphatases that turn off G proteins by dephosphorylating Gα. (b) the activity of phosphatases that turn GTP into GDP.(c) the degradation of the G protein after Gα separates from Gβγ(d) the GTPase activity of Gα

the GTPase activity of Gα

Proteins that are fully translated in the cytosol do not end up in (a) the cytosol. (b) the mitochondria. (c) the interior of the nucleus. (d) transport vesicles.

transport vesicles