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Biology 2382B Lecture Notes - Lecture 8: Cdk Inhibitor, Retinoblastoma Protein, E2F

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pearbuffalo731
10 Mar 2018
School
Western University
Department
Biology
Course
Biology 2382B
Professor
Robert Cumming

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Document Summary

Start or restriction point regulation by rb protein. Rb: retinoblastoma protein which is inactivated in many cancers. E2f transcription factor complex: binds to promoters upstream g1/s cyclin genes and. If dna damage is small -> dna repair enzymes, if dna damage is large -> apoptosis. Transcriptional regulation: turn on/off the expression of cyclins: e. g. Ubiquitin ligases: degrade and remove cyclins: e. g. Apc degrades mitotic cyclins, scf degrades g1 and s phase cyclins. Cyclin-dependent kinase inhibitors (cip): p21 and s phase inhibitor. Cdk: a kinase that phosphorylates things involved in mitosis to activate or inhibit them.

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Related Questions

1. You are interested in studying the cell cycle and have joineda lab to do so.

A) A student in the lab has taken the genes encoding for Cdk andM-cyclin, expressed them separately in bacteria, purified largequantities of both proteins, and then added them together to form apure M cyclin-Cdk complex. All these purification steps haveoccured smoothly, as assayed by protein gels he has run, and he isable to see a nice cyclin-Cdk complex forming. He decides to injectthe purified M cyclin-Cdk complex into oocytes that are notundergoing mitosis (like the experiment described in class). Hesees no effect of injecting purified M cyclin-Cdk into oocytes. Asa control, he also repeats the experiment described in class andinjects mitotic extract into oocytes and finds that the oocytesassemble a mitotic spindle (as expected). Given what you know aboutM cyclin-Cdk regulation, propose a reason for why his experimentmay not have worked? Be sure to explain youranswer.

B) A different graduate student has isolated mutants that aredefective in entry into S-phase. He has two alternative hypotheses:1) he has a mutation in S-cyclin such that it is unable to getdegraded in these mutants or 2) he has a mutation in E2F such thatit is unable to bind to Rb. Do you think either of these hypothesesmakes sense? Explain.