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Circadian Control of Cell Cycle Progression

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dc.contributor.authorSantos, Carlo Stevenen
dc.contributor.committeechairFinkielstein, Carla V.en
dc.contributor.committeememberHuckle, William R.en
dc.contributor.committeememberCapelluto, Daniel G. S.en
dc.contributor.departmentBiologyen
dc.date.accessioned2017-04-04T19:50:47Zen
dc.date.adate2009-06-12en
dc.date.available2017-04-04T19:50:47Zen
dc.date.issued2009-03-31en
dc.date.rdate2016-10-18en
dc.date.sdate2009-05-07en
dc.description.abstractTumorigenesis is the result of uncontrolled cell growth due to the deregulation of cell cycle checkpoints 1. Period 2 (Per2) is a tumor suppressor that oscillate in expression in a 24-hour cycle 2, 3. Here, we show that Per2 interacts with the tumor suppressor protein p53. Both G1 and G2 checkpoint pathways involve a p53 dependent pathway which can trigger the cell to go through cell arrest or programmed cell death4. Understanding all the mitigating factors involved in regulating cell cycle progression under DNA damage can offer a better idea in how cells become immortal. Initially discovered through screening of a human liver cDNA library, the novel interaction between p53-Per2 was further documented using co-precipitation. Interestingly, under genotoxic stress conditions, p53 and Per2 were not found to bind which leads us to suspect that Per2 does not affect active p53 which may possibly be due to post translational modifications of its active state. Furthermore we investigated p53's ability to act as a transcription factor in the presence of Per2, showing that the Per2-p53 complex prevents p53 from binding to DNA. This implies that the tetramerization of p53 may also be another factor in Per2's ability to bind to p53. A truncated p53 lacking the last 30 amino acids that theoretically increase p53's ability to form a tetramer showed a drastic reduction in binding to Per2 5, 6. On the other hand, p53 lacking the tetramerization domain showed binding similar to wildtype. Consequently we speculate that the ability of Per2 to modulate p53 and act as a tumor suppressor protein may be dependent on either the post translational modifications of p53 or its oligomeric state.en
dc.description.degreeMaster of Scienceen
dc.identifier.otheretd-05072009-221538en
dc.identifier.sourceurlhttp://scholar.lib.vt.edu/theses/available/etd-05072009-221538/en
dc.identifier.urihttp://hdl.handle.net/10919/76987en
dc.language.isoen_USen
dc.publisherVirginia Techen
dc.rightsIn Copyrighten
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/en
dc.subjectPeriod-2en
dc.subjectp53en
dc.subjectcircadianen
dc.subjectcheckpointen
dc.titleCircadian Control of Cell Cycle Progressionen
dc.typeThesisen
dc.type.dcmitypeTexten
thesis.degree.disciplineBiologyen
thesis.degree.grantorVirginia Polytechnic Institute and State Universityen
thesis.degree.levelmastersen
thesis.degree.nameMaster of Scienceen

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