Dulic lecture notes - G1-S transition Background A. Control...

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1 G1-S transition Background A. Control of cdk activity 1. cyclin •cyclin association is necessary but not sufficient for cdk activity. •cyclin dictates substrate specificity of the cdk 2. cdk •Phosphorylation and dephosphorylation of the cdk provides additional control. •Today, we examine a third type of control provided by the "CKI" or "cdk inhibitor". B. DNA damage is a catastrophic event that delays progression in the cell cycle. •Delay provides time for DNA repair or initiating programmed cell death. •In multicellular organisms, the real danger in mutating the DNA of a cell is not that the cell will die but that the cell may acquire uncontrolled proliferative capacity and could become cancerous.
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2 Dulic et al. (1994) p53-dependent inhibition of cyclin-dependent kinase activities in human fibroblasts during radiation-induced G1 arrest. Cell 76:1013-1023. A. Major Questions •What is the mechanism whereby cells delay the cell cycle in response to DNA damage? B. Hypothesis •Cells down-regulate cyclin-cdk complexes involved in G1/S transition in response to DNA damage •cyclin D •cyclin E •cyclin A?
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3 C. Approach: Biochemistry/ Immunoprecipitations / Cell culture Experimental Strategy: •Does cyclin-cdk complex activity in G 1 -S decrease in response to γ -ray-induced DNA damage?
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This note was uploaded on 10/19/2009 for the course B M B 460 taught by Professor Hanna-rose,w during the Spring '08 term at Pennsylvania State University, University Park.

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Dulic lecture notes - G1-S transition Background A. Control...

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