title: SIP1 is a catabolite repression-specific negative regulator of GAL gene expression.
abstract: The yeast Snf1p kinase is required for normal expression of many genes involved in utilization of non-glucose carbon. Snf1p is known to associate with several proteins. One is Sip1p, a protein that becomes phosphorylated in the presence of Snf1p and thus is a candidate Snf1p kinase substrate. We have isolated the SIP1 gene as a multicopy suppressor of the gal83-associated defect in glucose repression of GAL gene expression. Multicopy SIP1 also suppressed the gal82-associated defect in glucose repression, suggesting that SIP1, GAL83 and GAL82 function interdependently. Multicopy SIP1 gene reduces GAL1, GAL2, GAL7 and GAL10 gene expression three- to fourfold in cells grown in the presence of glucose but has no effect in cells grown on nonrepressing carbon. Sip1-deletion cells exhibited a two- to threefold increase in GAL gene expression compared to wild-type cells when grown on glucose. These studies show that SIP1 is a catabolite repression-specific negative regulator of GAL gene expression. Northern analysis revealed two SIP1 transcripts whose relative abundance changed with carbon source. Western blots revealed that Sip1p abundance is not markedly affected by carbon source, suggesting that Sip1p may be regulated post-translationally.
authors.affiliation: Department of Biochemistry and Molecular Biology, Pennsylvania State University College of Medicine, Hershey 17033.
authors.forename: L M
authors.initials: LM
authors.lastname: Mylin
authors.forename: V L
authors.initials: VL
authors.lastname: Bushman
authors.forename: R M
authors.initials: RM
authors.lastname: Long
authors.forename: X
authors.initials: X
authors.lastname: Yu
authors.forename: C M
authors.initials: CM
authors.lastname: Lebo
authors.forename: T E
authors.initials: TE
authors.lastname: Blank
authors.forename: J E
authors.initials: JE
authors.lastname: Hopper
mesh_terms: D055372:AMP-Activated Protein Kinases; D001483:Base Sequence; D002352:Carrier Proteins; D004794:Enzyme Repression / Q000235:genetics; D005656:Fungal Proteins / Q000235:genetics* / Q000378:metabolism; D005686:Galactokinase / Q000096:biosynthesis; D005690:Galactose / Q000378:metabolism; D017353:Gene Deletion; D015966:Gene Expression Regulation, Fungal; D005800:Genes, Fungal; D016153:Genes, Suppressor; D005947:Glucose / Q000378:metabolism; D008969:Molecular Sequence Data; D005810:Multigene Family; D011494:Protein Kinases / Q000378:metabolism; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D012097:Repressor Proteins / Q000235:genetics; D015183:Restriction Mapping; D012441:Saccharomyces cerevisiae / Q000201:enzymology* / Q000235:genetics; D029701:Saccharomyces cerevisiae Proteins; D015398:Signal Transduction / Q000235:genetics; D013379:Substrate Specificity; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D002352:Carrier Proteins; D005656:Fungal Proteins; C085569:GAL83 protein, S cerevisiae; D012097:Repressor Proteins; D029701:Saccharomyces cerevisiae Proteins; D014157:Transcription Factors; D011494:Protein Kinases; C071570:SNF1-related protein kinases; D005686:Galactokinase; D017346:Protein Serine-Threonine Kinases; C075934:SIP1 protein, S cerevisiae; C078651:SNF4 protein, S cerevisiae; D055372:AMP-Activated Protein Kinases; D005947:Glucose; D005690:Galactose