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dc.contributor.authorBlaire, Rachael Haley
dc.creatorBlaire, Rachael Haleyen_US
dc.date.accessioned2011-10-24T16:42:58Z
dc.date.available2011-10-24T16:42:58Z
dc.date.issued2010-05
dc.identifier.citationBlaire, Rachael Haley. (2010). The Role of the Rck1 and Rck2 Kinases in the Osmotic Stress Response of Budding Yeast (Bachelor's thesis, University of Arizona, Tucson, USA).
dc.identifier.urihttp://hdl.handle.net/10150/146568
dc.description.abstractIn response to high extracellular salt levels, Saccharomyces cerevisiae activates the HOG1 mitogen-activated protein kinase (MAPK) cascade, which signals to decrease cell growth and provide a method of survival in osmotic stress. Studies have shown that this occurrence can be attributed to an interaction between Hog1 and TOR (target of rapamycin); however, the method of interaction is unknown. Here, we use microarrays to investigate Rck2, a direct downstream substrate of Hog1, and its close homologue Rck1, as possible intermediates connecting Hog1 and TOR in the osmotic stress response. Our findings demonstrated that Rck1 and Rck2 were not acting in a salt dependent manner; however knocking out these kinases did cause significant changes in gene expression at 2452 genes. Rather, using a gene ontology search program, we found that Rck1 and Rck2 are involved in regulating cell growth, and that they interact with 7 transcription factors: Fhl1, Rap1, Ino2, Hir1, Hir2, Spt2 and YML081W.
dc.language.isoenen_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/
dc.titleThe Role of the Rck1 and Rck2 Kinases in the Osmotic Stress Response of Budding Yeasten_US
dc.typetexten_US
dc.typeElectronic Thesisen_US
thesis.degree.grantorUniversity of Arizonaen_US
thesis.degree.levelbachelorsen_US
thesis.degree.disciplineHonors Collegeen_US
thesis.degree.disciplineMolecular and Cellular Biologyen_US
thesis.degree.nameB.S.en_US
refterms.dateFOA2018-05-27T19:21:24Z
html.description.abstractIn response to high extracellular salt levels, Saccharomyces cerevisiae activates the HOG1 mitogen-activated protein kinase (MAPK) cascade, which signals to decrease cell growth and provide a method of survival in osmotic stress. Studies have shown that this occurrence can be attributed to an interaction between Hog1 and TOR (target of rapamycin); however, the method of interaction is unknown. Here, we use microarrays to investigate Rck2, a direct downstream substrate of Hog1, and its close homologue Rck1, as possible intermediates connecting Hog1 and TOR in the osmotic stress response. Our findings demonstrated that Rck1 and Rck2 were not acting in a salt dependent manner; however knocking out these kinases did cause significant changes in gene expression at 2452 genes. Rather, using a gene ontology search program, we found that Rck1 and Rck2 are involved in regulating cell growth, and that they interact with 7 transcription factors: Fhl1, Rap1, Ino2, Hir1, Hir2, Spt2 and YML081W.


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