SIT4 regulation of Mig1p-mediated catabolite repression in Saccharomyces cerevisiae

Can Jin, Antoni Barrientos, Charles B. Epstein, Ronald A. Butow, Alexander Tzagoloff

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)5658-5663
Number of pages6
JournalFEBS letters
Volume581
Issue number29
DOIs
StatePublished - Dec 11 2007
Externally publishedYes

Keywords

  • Catabolite repression
  • MIG1
  • Mitochondria
  • Respiration
  • Saccharomyces cerevisiae
  • SIT4

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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