SIP1 is a Catabolite Repression-Specific Negative Regulator of GAL Gene Expression

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The yeast Snflp kinase is required for normal expression of many genes involved in utilization of non-glucose carbon. Snflp is known to associate with several proteins. One is Sip1p, a protein that becomes phosphorylated in the presence of Snflp and thus is a candidate Snflp 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 Siplp abundance is not markedly affected by carbon source, suggesting that Siplp may be regulated post-translationally.

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