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WVSOM
Cell Cycle Control
| Question | Answer |
|---|---|
| Somatic cell division | Mitosis |
| All periods of the cell cycle except mitosis or meiosis | Interphase |
| The period following mitosis or meiosis with no DNA replication | G1 phase |
| An arrested G1 phase. Cells which cease to divide are usually in this phase permanently. | G0 phase |
| The period of DNA replication | S phase |
| The period between the completion of DNA replication and the onset of mitosis | G2 phase |
| Major cell cycle regulatroy proteins. They become abundant during the stage when they act, and they are degraded at the end of their stage. Degradation of these proteins allows the cell cycle to progess to the next stage. | Cyclins |
| Cyclins expressed during G1 stage, controlling progression from G1 to S phase | G1 Cyclins, e.g. C,D,E |
| Cyclins expressed during G2 to Mitosis stages, controlling progression from G2 to mitosis | G2 Cyclins, e.g. A,B |
| Kinases that are activated by cyclin binding. Their levels do not change during the cell cycle. However, do do cyclin binding their enzymatic activities do. | Cyclin Dependent Kinases (CDKs) |
| These proteins phophorylate specific threonine and tyrosine residues of specific proteins thereby inducing cell cycle progression | CDKs |
| Bound and activated by G1 cyclins | G1 CDKs, e.g. Cdk2, Cdk4 |
| Bound and activated by G2 cyclins | G2 CKS, e.g. cdc2 |
| G2 cyclin/cdc2 complex which induces mitosis by phophorylating components such as nuclear lamins and H1 histones | Mitotic Promoting Factor (MPF) |
| cdc2 kinase activity activated by G2 cyclin binding | MPF activity |
| Signals to decide whether to progress with the cell cycle. | Checkpoints |
| This checkpoint induces the rapid onset of mitosis when MPF complexes reach a threshold concentration | cdc25 |
| Factors that normally function to inhibit cell cycle progression. | Tumor Suppressors |
| Factors that normally function to promote cell cycle progression | Oncogenes (really proto-oncogenes) |
| A tumor suppressor gene that blocks progress from G1 to S phase. Hyperphosphorylation of this gene causes it to release a factor known as EF2. | Retinoblastoma (Rb) |
| A transcription factor that induces progression to S shase by activating expression of genes required for DNA replication. Also activates transcription of its own gene. | EF2 |
| A tumor suppressor that responds to DNA damage and certain oncogens, by either blocking cell cycle progression or inducing apoptosis. A transcription factor. Normally it is degraded by the ubiquitin pathway. | p53 |
| A general inhibitor of all G1 and G2, cyclin/CDK complexes whose transcription factor is p53. | p21 |
| There is no gene which can produce cancer by itself. Three or more gens must be mutated or deregulated before a cell will divide out of control. | Multiple Hit Hypothesis |
Created by:
mhaynes
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