Analysis of the mechanism by which glucose inhibits maltose induction of MAL gene expression in Saccharomyces

Expression of the MAL genes required for maltose fermentation in Saccharomy ces cerevisiae is induced by maltose and repressed hy glucose. Maltose-indu cible regulation requires maltose permease and the MAL-activator protein, a DNA-binding transcription factor encoded by MAL63 and its homologues at th e other MAL loci. Previously, we showed that the Mig1 repressor mediates gl ucose repression of MAL gene expression. Glucose also blocks MAL-activator- mediated maltose induction through a Mig1p-independent mechanism that we re fer to as glucose inhibition. Here we report the characterization of this p rocess. Our results indicate that glucose inhibition is also Mig2p independ ent. Moreover, we show that neither overexpression of the MAL-activator nor elimination of inducer exclusion is sufficient to relieve glucose inhibiti on, suggesting that glucose acts to inhibit induction by affecting maltose sensing and/or signaling. The glucose inhibition pathway requires HXK2, REG 1, and GSF1 and appears to overlap upstream with the glucose repression pat hway. The likely target of glucose inhibition is Snf1 protein kinase. Evide nce is preserved indicating that, in addition to its role in the inactivati on of Mig1p, Snf1p is required posttranscriptionally for the synthesis of m altose permease whose function is essential for maltose induction.