Glucose represses the lactos-galactose regulon in Kluyveromyces lactis through a SNF-1 and MIG1-dependent pathway that modulates galactokinase (GAL1) gene expression

Expression of the lactose-galactose regulon in Kluyveromyces lactis is induced by lactose or galactose and repressed by glucose. Some components of the induction and glucose repression pathways have been identified but many remain unknown. We examined the role of the SNF1 (KISNF1) and MIG1 (KIMIG1) genes in the induction and repression pathways. Our data show that full induction of the regulon requires SNF1; partial induction occurs in a Klsnf1-deleted strain, indicating that a KISNF1-independent pathway(s) also regulates induction. MIG1 is required for full glucose repression of the regulon, but there must be a KIMIG1-independent repression pathway also. The KIMig1 protein appears to act downstream of the KISnf1 protein in the glucose repression pathway. Most importantly, the KISnf1-KIMig repression pathway operates by modulating KIGAL1 expression. Regulating KIGAL1 expression in this manner enables the cell to switch the regulon off in the presence of glucose. Overall, our data show that, while the Snf1 and Mig1 proteins play similar roles in regulating the galactose regulon in Saccharomyces cerevisiae and K. lactis, the way in which these proteins are integrated into the regulatory circuits are unique to each regulon, as is the degree to which each regulon is controlled by the two proteins.