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Chapter 17-18 & 20 Quiz Practice

Terms in this set (25)

Describe the mechanisms that control the (a) start, (b) G2/M and (c) metaphase-anaphase transition steps in cell cycle. What are the similarities and differences between these three regulatory mechanisms?
- Cdk kinases are the master controllers that regulate the transition of the phases of the cell cycle
- Cyclins are the activators of those kinases
- Cyclins are expressed cyclically
What is APC/C?
- APC/C is a ubiquitin ligase
- marks protein for destruction by the proteasome
What does APC/C do?
- targets protease inhibitor securin for destruction
- without securin, seperase becomes active and cleaves cohesins
- APC/C also targets Cdks, leading to the loss of phosphorylation on Cdk targets - necessary for completion of mitosis and cytokinesis
M-Cdk drives entry into Mphase. There is a raid increase in m-Cdk activity at G2-M transition. However, M cyclin increases gradually throughout G2. If M cyclin is the activator of M-Cdk, how can this gradual increase of M cyclin lead to such a rapid rise M-Cdk activity at the G2-M transition? Describe the mechanism in detail (or diagram).
- Complexes of M-cyclin and M-cdk accumulat throughout G2
- But the complexes are not active due to inhibitory phosphorylation by Wee1 kinase
What is M-Cdk?
- Cdk1-M-cyclin complexes inhibited by phosphorylation of Wee1 kinase
- Activation of M-Cdk activity requires dephosphorylation by Cdc-25
- Cdc-25 activated at the G2-M transition
- positive feedback - active M-Cdk activates Cdc25
- positive feedback - MCdk inhibits Wee1 (activating kinase)
Which cells in figure Q17.1 are in G1, S, G2, and M phases of the cell cycle?
G1: at peak 1
S: in middle
G2: at peak 2
- block the cell in G1
- during S phase, the S and G2 phase are in place
- G2/M before cytokinesis
Expression of Scc1 at the beginning of S phase leads to normal division. Expression of both is completed, cells do not divide and die. WHY?
- if the sister chromatids are not attached to each other as replication occurs, they will become a tangled mess. Likely impossible to untangle once replication is finished
Compare and Contrast the intrinsic versus extrinsic apoptotic pathways. Be specific as to the molecular mechanisms that mediate these modes of cell death.
- Both involve an intracellular proteolytic cascade mediated by caspases
- Extrinsic: initiated by cell surface receptors (Fas, TNF alpha)
- intrinsic: involves the release of proteins from the mitochondrial matrix
What happened to cytochrome C in a mitochondrial matrix?
- cytochrome C released
- Cytochrome C, Apaf 1, assembly of the apoptosome
- activation of caspase 9 initiator caspase
Which family regulate intrinsic pathway?
- Bcl2 family proteins
- both pro-apoptotic and anti-apoptotic Bcl2 proteins
Why the difference between Apaf1-/- and Caspase 9-/- mutants?
- must be other caspases they can mediate this apoptotic mechanism
- no effect on interdigital webbing was seen with caspase 3 or 9 knocked out mice, which suggests that Apaf-1 regulates the activation of additional caspases
Do cells slowly release Cyt C over hours. Or do cells release Cyt C quickly, but different cells are triggered over a long period of time, so the release in a population of cells is seen as slow?
- released within minutes (6,8)
- GFP is a method that allows experiments at the single cell level
What fraction would be Fas-Fas complexes would be 100% normal Fas (in Het)?
1/2 X 1/2 X 1/2 = 1/8 normal fas receptor complexes
What fraction for het with deletion allele?
100% normal fas receptor complexes
is het for deletion normal?
YES, should be normal!
What can be concluded about the number of mutations required for cancer onset from the figure at right?
- if a single mutation caused cancer you would expect the frequency of cancer to match the frequency of mutation rates. (Over human lifetime every gene in human should have undergone mutation about 10^10 times)
- The frequency of cancer would be independent of age
- cancer caused by a progressive, random accumulation of a set mutations in a single lineage of cells
What can be concluded about the timing of cancer onset from the figure at right? What might explain that?
long delay (35 years). Cancer requires multiple things to go wrong. Cancer cell goes through a succession of changes
Name 3 mechanisms by which a proto-oncogene can be converted to an oncogene.
- deletion or point mutation in coding sequence
- regulatory mutation
- gene amplification
- chromosome rearrangement
In many overactive ways gene mutated in cancer:
- extracellular domain of receptor
- binding of growth factor triggers intracellular signaling
- truncated receptor triggers intracellular signaling in absence of growth factor
What is the generalized function of the genes listed in the figure below?
Methylation turns off the expression
Why would hypermethylation of these genes lead to cancer?
tumor suppressors
What was measured to make this figure?
Mutation rates for specific genes across many tumors (colorectal cancer)
What is the conclusion for this figure? (tumor cells are merely passengers)
- High frequency mutations expected to be causal or driver mutations
- other could be just passengers (not involved in onset)
Results for transgenic mice experiments are shown in the graph at right. What was the experiment?
- Made transgenic mice expressing oncogene versions of these genes
- synergistic effect shows that oncogenes collaborate
What is the conclusion? (Cancer Critical Gene)
the rate of cancer with both mutant genes is higher than the sum of rates of each alone
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