Hypertonic shock and the cell cycle: Identification of a stress-induced G2 delay in Saccharomyces cerevisiae

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dc.contributor.advisorGustin, Michael C.en_US
dc.creatorAlexander, Matthew Roberten_US
dc.date.accessioned2009-06-04T08:17:22Zen_US
dc.date.available2009-06-04T08:17:22Zen_US
dc.date.issued1999en_US
dc.description.abstractExposure of S. cerevisiae cells to an increase in external osmolarity induces a temporary growth arrest. Recovery from this stress is mediated by the accumulation of intracellular glycerol and the transcription of several stress response genes. This study demonstrates that an additional effect is the triggering of a cell cycle delay during G2/M. Increasing the extracellular osmolarity results in an accumulation of 1N and 2N cells, and a depletion of S phase cells from an asynchronous culture. Additionally, hypertonic stress causes a decrease in mRNA from the B-type cyclin CLB2, phosphorylation of the cyclin dependent kinase Cdc28p, and inhibition of Clb2p-Cdc28p kinase activity, while Clb2 protein levels are unaffected. The osmotic stress induced G2 delay is dependent upon the kinase Swe1p. Surprisingly, this delay is not correlated with inhibition of Clb2p-Cdc28p kinase activity. Deletion of SWE1 prevents the phosphorylation of Cdc28p in response to hypertonic shock, and removes the block to cell cycle progression. Deletion of SWE1 also causes synchronized cultures stressed in G2 to accumulate cells with mislocalized nuclei. However, deletion of SWE1 does not prevent the hypertonic stress induced inhibition of Clb2p-Cdc28p kinase activity. Conversely, deletion of HOG1 does prevent Clb2p-Cdc28p inhibition, but does not block Cdc28p phosphorylation or significantly remove the block to cell cycle progression. Deletion of HOG1 does however further disrupt post-stress nuclear localization in combination with a swe1Delta mutation. Finally, preventing Cdc28p phosphorylation by a Y19F substitution does not disrupt the cell cycle delay to the same degree as deletion of SWE1. Together, these results suggest that osmotic stress-induced cell cycle delay is mediated in a novel way by Swe1p, with a contribution from the MAP kinase Hog1p.en_US
dc.format.extent168 p.en_US
dc.format.mimetypeapplication/pdfen_US
dc.identifier.callnoTHESIS BIOCHEM. 1999 ALEXANDERen_US
dc.identifier.citationAlexander, Matthew Robert. "Hypertonic shock and the cell cycle: Identification of a stress-induced G2 delay in Saccharomyces cerevisiae." (1999) Diss., Rice University. <a href="https://hdl.handle.net/1911/19346">https://hdl.handle.net/1911/19346</a>.en_US
dc.identifier.urihttps://hdl.handle.net/1911/19346en_US
dc.language.isoengen_US
dc.rightsCopyright is held by the author, unless otherwise indicated. Permission to reuse, publish, or reproduce the work beyond the bounds of fair use or other exemptions to copyright law must be obtained from the copyright holder.en_US
dc.subjectMolecular biologyen_US
dc.subjectCell biologyen_US
dc.titleHypertonic shock and the cell cycle: Identification of a stress-induced G2 delay in Saccharomyces cerevisiaeen_US
dc.typeThesisen_US
dc.type.materialTexten_US
thesis.degree.departmentBiochemistry and Cell Biologyen_US
thesis.degree.disciplineNatural Sciencesen_US
thesis.degree.grantorRice Universityen_US
thesis.degree.levelDoctoralen_US
thesis.degree.nameDoctor of Philosophyen_US
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