The GCR1 gene function is essential for glycogen and trehalose metabolism in Saccharomyces cerevisiae
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
12630316
DOI
10.1007/bf02818668
Knihovny.cz E-resources
- MeSH
- DNA-Binding Proteins genetics metabolism MeSH
- Fungal Proteins genetics metabolism MeSH
- Glucan 1,4-alpha-Glucosidase metabolism MeSH
- Glycogen biosynthesis metabolism MeSH
- Mutation genetics MeSH
- Saccharomyces cerevisiae Proteins MeSH
- Saccharomyces cerevisiae genetics metabolism MeSH
- Transcription Factors MeSH
- Trehalase metabolism MeSH
- Trehalose biosynthesis metabolism MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- DNA-Binding Proteins MeSH
- Fungal Proteins MeSH
- GCR1 protein, S cerevisiae MeSH Browser
- Glucan 1,4-alpha-Glucosidase MeSH
- Glycogen MeSH
- Saccharomyces cerevisiae Proteins MeSH
- Transcription Factors MeSH
- Trehalase MeSH
- Trehalose MeSH
Trehalose (Tre) and glycogen (Glg) are synthesized in response to unfavorable growth conditions from glycolytic intermediates in Saccharomyces cerevisiae. Transcription of the glycolytic genes is activated by the Gcr1p complex, the DNA binding transcription factor that directly associates with the CT-box sequences on the promoter region of the glycolytic genes. gcr1 mutant yeast cells cannot utilize glucose effectively. Glg and Tre levels in stationary-phase gcr1 mutant yeast cells were 20-50% of those in the wild-type strain. Likewise, stress-induced accumulation of Tre and Glg in gcr1 mutant cells was significantly lower than in the wild type. In addition, both the synthesis and the degradation of Tre and Glg are very slow in the gcr1 mutant. It seems that Gcr1p function is essential for the coordinated regulation of glycolysis, Tre and Glg metabolism in S. cerevisiae.
See more in PubMed
J Cell Biol. 1999 May 31;145(5):979-91 PubMed
Genetics. 2000 Nov;156(3):1005-23 PubMed
Genetics. 2001 Jan;157(1):39-51 PubMed
FEBS Lett. 1993 Aug 23;329(1-2):51-4 PubMed
J Bacteriol. 2000 Sep;182(17):4970-8 PubMed
Yeast. 1999 Aug;15(11):1045-57 PubMed
Genetics. 1996 May;143(1):57-66 PubMed
FEMS Microbiol Rev. 2001 Jan;25(1):125-45 PubMed
Yeast. 1999 Feb;15(3):191-203 PubMed
Curr Genet. 1993;23(4):281-9 PubMed
Crit Rev Biochem Mol Biol. 1993;28(4):259-308 PubMed
Microbiology (Reading). 1997 Jun;143 ( Pt 6):1891-1900 PubMed
Anal Biochem. 1997 May 15;248(1):186-8 PubMed
Genetics. 1997 Oct;147(2):493-505 PubMed
Genetics. 2001 May;158(1):133-43 PubMed
Trends Biochem Sci. 1995 Jan;20(1):3-10 PubMed
Yeast. 1997 Aug;13(10):917-30 PubMed
J Bacteriol. 1999 Jan;181(2):396-400 PubMed
Folia Microbiol (Praha). 1999;44(4):372-6 PubMed
J Bacteriol. 1980 Sep;143(3):1384-94 PubMed
J Bacteriol. 1997 Nov;179(21):6560-5 PubMed
Genetics. 1978 Jan;88(1):1-11 PubMed
Mol Cell Biol. 1986 Nov;6(11):3774-84 PubMed
Mol Cell Biol. 1996 Aug;16(8):4357-65 PubMed
FEMS Microbiol Lett. 1993 Apr 15;108(3):333-9 PubMed
Mol Cell Biol. 1993 Jan;13(1):543-50 PubMed