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dc.contributor.authorZhou, Heng
dc.contributor.authorWinston, Fred Marshall
dc.date.accessioned2010-11-01T17:53:45Z
dc.date.issued2001
dc.identifier.citationZhou, Heng and Fred Winston. 2001. NRG1 is required for glucose repression of the SUC2 and GAL genes of Saccharomyces cerevisiae. BMC Genetics 2:5.en_US
dc.identifier.issn1471-2156en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:4515096
dc.description.abstractBackground: Glucose repression of transcription in the yeast, Saccharomyces cerevisiae, has been shown to be controlled by several factors, including two repressors called Mig1 and Mig2. Past results suggest that other repressors may be involved in glucose repression. Results: By a screen for factors that control transcription of the glucose-repressible SUC2 gene of S. cerevisiae, the NRG1 gene was identified. Analysis of an nrg1Δ mutant has demonstrated that mRNA levels are elevated at both the SUC2 and of the GAL genes of S. cerevisiae when cells are grown under normally glucose-repressing conditions. In addition, genetic interactions have been detected between nrg1Δ and other factors that control SUC2 transcription. Conclusions: The analysis of nrg1Δ demonstrates that Nrg1 plays a role in glucose repression of the SUC2 and GAL genes of S. cerevisiae. Thus, three repressors, Nrg1, Mig1, and Mig2, are involved as the downstream targets of the glucose signaling in S. cerevisiae.en_US
dc.description.sponsorshipMolecular and Cellular Biologyen_US
dc.language.isoen_USen_US
dc.publisherBioMed Centralen_US
dc.relation.isversionofdoi:10.1186/1471-2156-2-5en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC31344/pdf/en_US
dash.licenseLAA
dc.titleNRG1 is Required for Glucose Repression of the SUC2 and GAL Genes of Saccharomyces Cerevisiaeen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalBMC Geneticsen_US
dash.depositing.authorWinston, Fred Marshall
dc.date.available2010-11-01T17:53:45Z
dc.identifier.doi10.1186/1471-2156-2-5*
dash.contributor.affiliatedWinston, Fred


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