Lect9_CellCycle2

Lect9_CellCycle2 - Go (Stationary) Phase, and re-entry to...

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G o (Stationary) Phase, and re-entry to the cell cycle Most cells in the body are differentiated to enable them to carry out specialized functions . Terminal differentiation requires that cells exit the cell cycle . Such cells are considered to be in an unique compartment of G 1 termed G 0 . Cells in G 0 phase are not dormant - they are usually actively engaged in protein synthesis and secretion and can be motile. G 0 is not necessarily permanent some cells can be recruited to re-enter cell cycle if given appropriate stimuli , which is often exposure to mitogens (see below) Cells in multi-cellular organisms divide only when required; i.e. the default state is not to divide . Growth factors - Stimulate increase in cell mass by promoting synthesis and inhibiting degradation of macromolecules. Mitogens - stimulate cell division by relieving negative controls that block cell cycle progression, especially in G 1 . Some factors simultaneously promote both processes . Mitogens required even for cells NOT in G 0 Growth factors and mitogens are extracellular!! 1 Bio 103-Fall 2009 © Steven Gross
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Growth factors - extracellular factors that stimulate cell growth 2 Growth factors bind to extracellular receptors . Activate phosphoinositol-3-kinase (plus other pathways). Activates downstream kinases - e.g. TOR. eIF4E is rate limiting in translation of mRNA. Increase in steady-state level of eIF4E and S6 leads to rapid increase in synthesis of proteins and molecules required for cell metabolism and cell growth . Bio 103-Fall 2009 © Steven Gross
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3 Binds to extracellular receptors . Activate MAP kinase pathways. MAPK mediates transcription of myc , which encodes a transcription factor . Myc increases levels of G 1 -cyclin , which activates G 1 -cdk . Non-phosphorylated Rb -protein binds and sequesters transcription factor E2F , thereby blocking expression of genes required for growth . Activated G 1 -cyclin /cdk phosphorylates Rb protein , which causes inactivation of Rb . E2F now mediates expression of genes required for cell to progress through G 1 to begin DNA replication and cell division . S-phase cyclins synthesized in G1, but are inactive due to binding by inhibitor , Sic1 . Mitogens - extracellular factors that stimulate cell division Bio 103-Fall 2009 © Steven Gross Removal of Sic1
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4 S-phase cyclins synthesized in G1, but are inactive due to binding by inhibitor , Sic1 . Activation of S-phase cyclins Bio 103-Fall 2009 © Steven Gross To Activate S-phase cyclins: 1. When concentration of G1 cyclins is relatively high , they result in removal of Sic1 from S-CDK by phosphorylating Sic1 2. Destruction of Sic1 by SCF-mediated ubiquitination and degradation Sic1 Inactive Sic1- S-CDK complex Removal of Sic1
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Consequence of loss of negative regulator of G 1 - retinoblastoma Loss of function of Rb (retinoblastoma) gene product.
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This note was uploaded on 12/13/2011 for the course BIOSCI d103 taught by Professor Staff during the Fall '11 term at UC Irvine.

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Lect9_CellCycle2 - Go (Stationary) Phase, and re-entry to...

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