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SIT4 regulation of Mig1p‐mediated catabolite repression in Saccharomyces cerevisiae
Author(s) -
Jin Can,
Barrientos Antoni,
Epstein Charles B.,
Butow Ronald A.,
Tzagoloff Alexander
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.11.027
Subject(s) - catabolite repression , saccharomyces cerevisiae , repressor , psychological repression , mutant , fed batch culture , polysome , biochemistry , phosphorylation , phosphatase , derepression , transcriptional regulation , biology , chemistry , yeast , gene , gene expression , rna , ribosome , fermentation
E153 is a respiratory deficient mutant of Saccharomyces cerevisiae with a mutation in the active site of the Sit4p protein phosphatase. Measurements of mitochondrial respiration and cytochromes indicate that the mutation suppresses glucose repression. The escape from catabolite repression is accompanied by a marked reduction of the transcriptional repressor Mig1p. The presence of normal levels of MIG1 mRNA in the mutant and its association with the polysome fraction suggests that depletion of Mig1p is the result of protein degradation. This study shows that in addition to phosphorylation by Snf1p, the transcriptional repressor activity of Mig1p is also regulated by a post‐transcriptional Sit4p‐dependent pathway. Our evidence suggests that this pathway involves turnover of Mig1p.