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Answer each of the following with the most correct choice. Each problem has only one answer.

problem) during the cell cycle:
a.    DNA damage causes the E3 protein Mdm2 to ubiquitinate p53
b.    DNA damages cause destabilization of p53
c.    DNA damage triggers synthesis of p21, a CKI for G1/S—Cdk and S—cdk
d.    Different Cdk kinases are synthesized and degraded in a regulated manner
e.    A and B

problem) Cdk complexes can be regulated by the following mechanisms EXCEPT
a.    cyclin degradation
b.    cyclin synthesis
c.    phosphorylation
d.    CKI degradation
e.    None of the above

problem) Mutational inactivation of the Rb protein can lead to uncontrolled cell proliferation and retinoblastoma ( a form of cancer) because
a.    Too much mitogen signaling will occur
b.    The E2F transcription factor will be always active
c.    Inhibitory phosphorylation will not occur on Cdk complexes
d.    M—Cdk will not be inhibited
e.    None of the above

problem) What would be the effect of artificially DECREASING the activity of the Cdc25 phosphatase in a cell?
a.    The cell cycle would get longer
b.    M—Cdk would become active sooner
c.    The cell would get smaller
d.    The activation of APC/Cdc20 would occur faster
e.    The activating phosphorylation on Cdk complexes will not occur

problem) Cell cycle check points are
a.    Surveillance mechanisms that promote the activation of Cdk complexes
b.    Monitoring mechanisms that inhibit protein synthesis at specific times of the cell cycle
c.    Required for cell cycle progression
d.    Signaling mechanisms that stop cell cycle progression until specific conditions are met
e.    Important only after DNA damage

problem) Which of the following is TRUE regarding caspases?
a.    They are synthesized in response to apoptotic stimulus
b.    They are activated by phosphorylation
c.    They are present in all animal cells, but generally in their inactive forms
d.    They can be inhibited by anti—IAPs
e.    They are responsible for the cleavage of a few proteins

problem) Which of the following is NOT an essential part of the EXTRINSIC pathway of apoptosis
a.    Cytochrome c
b.    DISC
c.    Death receptor
d.    Death ligand
e.    Initiator caspase

problem) Which of the following is NOT a key feature of apoptosis
a.    Collapse of the cytoskeleton
b.    Nuclear envelope disassembly
c.    Cell lysis
d.    Chromosome fragmentation
e.    Changes in cell shape

problem) In animal cells, the nuclear envelope is dismantled during_____ and reformed during_____
a.    Interphase, prophase
b.    Prophase, anaphase
c.    Telophase, metaphase
d.    Prophase, telophase
e.    Metaphase, interphase

problem) Which of the following events occurs at the very beginning of M phase
a.    Degradation of M—cyclin through ubiquitination
b.    Synthesis of G1 cyclin through transcription and translation
c.    Phosphorylation of cohesin by M—cdk
d.    Beginning of association of cohesin with sister chromatids
e.    Phosphorylation of condensing by M--Cdk

problem) A cell can tell that its chromosomes have made CORRECT attachments to microtubles by
a.    Counting the number of microtubules that have attached to each kinetochore
b.    Detecting the positions of the kinetochores on the mitotic spindle
c.    Detecting tension between sister kinetochores
d.    Sensing the activity of chromokinesin
e.    None of the above

problem) Separation of MTOCs during prophase involves
a.    Minus end—directed motor at the cell cortex that works on (astral) microtubules
b.    Plus end—directed motor that works on interpolar microtubules from opposite poles
c.    Minus end—directed motor that works on interpolar microtubules from opposite poles
d.    Plus end—directed motor at kinetochore that works on kinetochore microtubules
e.    Minus end—directed motor at kinetochore that works on kinetochore microtubules

problem) GPCRs are used to control blood pressure by causing blood vessels to relax or contract. This process uses which of the following concepts
a.    Receptors are endocytosed via clathrin—coated vesicles to cause blood vessel relax
b.    Relaxing ligands signal for the blood vessels to relax
c.    Contraction of blood vessels requires two signaling pathways to interact in the cell while relaxation only requires one pathway
d.    One ligand can cause blood vessels to wither relax or contract depending on which G protein signaling pathway is activated
e.    None of the above

problem) After Gα hydrilyzes its GTP
a.    Signaling downstream of trimeric G protein will cease immediately
b.    GCPR will be endocytosed
c.    Gα will associate with Gβγ
d.    RGS protein will associate with Gα
e.    C and D

problem) Which of the following statements is FALSE regarding phospholipase C?
a.    It can generate second messengers
b.    It can generate PI(3,4,5)P3
c.    It can cleave off the polar head group of certain phosphoinoinositides
d.    It can be activated through GPCRs
e.    It can be activated through receptor tyrosine kinases

problem) Steroid sex hormones
a.    Bind GPCRs
b.    Are hydrophilic
c.    Lead to rapid responses in their target cells
d.    None of the above
e.    B and C

problem) Which of the following is NOT TRUE for protein kinase C (PKC)?
a.    It is activated by binding to diacylglycerol (DAG)
b.    It is activated by binding to calmodulin
c.    It is activated in response to phospholipase C activation
d.    It functions at or near a membrane
e.    It is often activated in response to GPCR activation

problem) Activation of PI 3—kinase at a site typically leads to the recruitment of proteins that contain
a.    Phosphorylated tyrosine residues
b.    Proline—rich regions
c.    SH2 domain
d.    Phosphorylated serine/threonine residues
e.    PH domain

problem) Induced proximity caused by ligand binding is used to activate
a.    Certain initiator caspases
b.    Many receptor kinases
c.    Many GPCRs
d.    All of the above
e.    A and B

problem) Binding of a ligand to a receptor tyrosine kinase (RTK) often causes the following EXCEPT:
a.    Autophosphorylation of RTK
b.    Recruitment of proteins with enzymatic activity to the RTK
c.    Activation of multiple downstream signaling pathways
d.    Activation of MAP kinase cascade
e.    Recruitment of RAS to the RTk

problem) Signaling through second messengers allows
a.    Amplification of extracellular signals
b.    The binding of ligand to receptos on the surface of one cell to generate responses in its neighboring cells in many instances
c.    Phospholipase C to be activated
d.    All of the above
e.    A and B

problem) For most cell types, the greatest total adhesive force with their neighbors comes from
a.    Cadherin
b.    Selectin
c.    IgSF protein
d.    Intefrin
e.    lectin

problem) Bacteria present in our gut do not readily invade our body because of
a.    Adherens junction present in epithelial cells
b.    Gap junctions present in epithelial cells
c.    Tight junctions present in epithelial cells
d.    Desmosomes present in epithelial cells
e.    Cell—matrix anchoring junction present in epithelial cells

problem) Which of the following adhesion molecules work mostly or exclusively through homotypic binding?
a.    Selectin
b.    Integrin
c.    Cadherin
d.    A and B
e.    B and C

problem) Which of the following is INCORRECT regarding chromokinesin?
a.    It is a plus end directed motor
b.    It is found mostly at kinetochores
c.    It works on interpolar microtubules
d.    It plays a role in congression
e.    None of the above (i.e, they are all correct)

Answer the following as either True or False

problem) During the cell cycle checkpoint in G2, the presence of unreplicated DNA results in the degradation of M—cyclin

problem)When a cell in M phase is fused to a cell in G1 phase, the chromosomes in the resulting fused cell will be condensed

problem) In some cells, the extrinsic apoptotic pathway utilizes the class C (BH3—only) protein Bid to amplify the caspase cascade to kill the cell

problem) A minus end—directed motor at the kinetochore is responsible for most of the forces needed during anaphase A

problem) Cam—Kinase that has been activated by calmodulin—binding will become inactive as soon as the calcium concentration in the cytosol drops

problem) Like monomeric G proteins, Gα of trimeric G proteins always binds effector proteins when it becomes GTP—bound

problem)Mutations in selectin are often found in metastatic cancer cells

problem)Mitogens very often work through a MAP kinase cascade

problem)Phagocytes recognize apoptotic cells because of the presence of phosphatidylcholine (PC) on the surface of apoptotic cells

problem)The main role of integrin in most cells is to cause cell—cell adhesion

problem) Fill in the blank with one or a small number of words

1) The function of E2F is to act as a _______ in the nucleus
2) Active caspase can cleave and activate ___ to cause collapse of the actin cytoskeleton
3) Sister chromatids are held together by___
4.) Receptors for IP3 are located at the ____
5) ____ can be cleaved to form archidonic acid, which can be further metabolized to cause inflammation
6) selectin has a lectin domain that binds_______
7) ______ functions as diffusion barriers for plasma membrane proteins.
8) The GEF for Gα is_______
9) Phosphorylation of _____ by M—Cdk is responsible for nuclear envelope breakdown
10) The position of the site of cytokinesis is dictated by the position of the ____ in most cell types

Essay problems:

problem) The cell—permeable small molecule MG132 is an inhibitor of the proteasome. You add this drug to cells that are in late G2. describe why this drug would or would not affect the following events and by which mechanism.. if there is an effect, describe which proteins will be affected and how this would change this particular event

a) Spindle assembly

i) MG132 will not affect spindle assemble.  Protein degradation is not a requirement for spindle assembly.  (For ex, the phosphorylation of nuclear lamins leads to fragmentation but not degradation) of the nuclear envelope.  This process is reversible, and dephosphorylation of lamins results in fusion of nuclear envelope fragments in telophase.)

b) Capturing of microtubules by kinetochores

c) Sister chromatid separation

i) MG132 will block chromatid separation. Normally, APC/C ubiquitinates securin, targeting it for degradation in the proteasome.  Thus, securin will not be degraded in the presence of MG132.  This would cause securin to remain bound to separase, keeping separase in an inactive state.  Inactive separase cannot cleave cohesin, resulting in an inhibition of chromatid separation.

problem) Severe DNA damage often leads to apoptosis via activation of the p53 transcription factor. Describe at the molecular level how p53 activation leads to apoptosis. You do NOT need to discuss any signaling from DNA damage to p53 activation

a) Exposure to cellular stress can trigger the p53 tumor suppressor, a sequence-specific transcription factor, to induce cell growth arrest or apoptosis. The choice between these cellular responses is influenced by many factors, including the type of cell and stress, and the action of p53co-activators. p53 stimulates a wide network of signals that act through two major apoptotic pathways. The extrinsic, death receptor pathway triggers the activation of a caspase cascade, and the intrinsic, mitochondrial pathway shifts the balance in the Bcl-2 family towards the pro-apoptotic members, promoting the formation of the apoptosome, and consequently caspase-mediated apoptosis. The impact of these two apoptotic pathways may be enhanced when they converge through Bid, which is a p53 target. The majority of these apoptotic effects are mediated through the induction of specific apoptotic target genes. However, p53 can also promote apoptosis by a transcription-independent mechanism under certain conditions. Thus, a multitude of mechanisms are employed by p53 to ensure efficient induction of apoptosis in a stage-, tissue- and stress-signalspecific manner. Manipulation of the apoptotic functions of p53 constitutes an attractive target for cancer therapy.

problem) At the onset of M phase, activation of a small amount of the Cdc25 phosphatase leads to very rapid conversion of a large amount of inactive M—Cdk complexes to active M—cdk complexes. Describe the feedback loops that allow this rapid accumulation to occur.

a) The activation of M-Cdk begins with the accumulation of M-cyclin. In embryonic cell cycles, the synthesis of M-cyclin is constant throughout the cell cycle, and M-cyclin accumulation results from a decrease in its degradation. In most cell types, however, M-cyclin synthesis increases during G2 and M, owing primarily to an increase in M-cyclin gene transcription. This increase in M-cyclin protein leads to a gradual accumulation of M-Cdk (the complex of Cdk1 and M-cyclin) as the cell approaches mitosis. Although the Cdk in these complexes is phosphorylated at an activating site by the enzyme CAK , it is held in an inactive state by inhibitory phosphorylation at two neighboring sites by the protein kinase Wee1 . Thus, by the time the cell reaches the end of G2, it contains an abundant stockpile of M-Cdk that is primed and ready to act, but the M-Cdk activity is repressed by the presence of two phosphate groups that block the active site of the kinase.

What, then, triggers the activation of the M-Cdk stockpile? The crucial event is the activation in late G2 of the protein phosphatase Cdc25, which removes the inhibitory phosphates that restrain M-Cdk. At the same time, the activity of the inhibitory kinase Wee1 is also suppressed, further ensuring that M-Cdk activity increases abruptly.

problem) Activated rhodopsin stimulates GRK to phosphorylate rhopsin itself. How does phosphorylated rhodopsin lead to desensitization?

a) As rhodopsin is phosphorylated by rhodopsin kinase (a member of the GPCR kinases(GRKs)), it binds with high affinity to the arrestin. The bound arrestin can contribute to the desensitization process in at least two ways. First, it prevents the interaction between the G protein and the activated receptor. Second, it serves as an adaptor protein to aid the receptor to the clathrin-dependent endocytosis machinery (to induce receptor-mediated endocytosis)

Biology, Academics

  • Category:- Biology
  • Reference No.:- M9304

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