REG2 encodes a regulatory subunit of the Glc7p type-1 protein phosphatase (PP1) (2). Reg2p, and the similar protein Reg1p, are each involved in targeting Glc7p to substrates that are phosphorylated by the Snf1p kinase (1). Glc7p-Reg2p and Glc7p-Reg1p are also involved in the glucose-induced proteolysis of maltose permease (Mal11p, Mal21p, Mal31p, Mal41p and Mal61p) (2).

Glucose repression of REG2 is partially dependent on Mig1p and Mig2p (4), and induction of REG2 expression during the diauxic shift is dependent on Cat8p (5). REG2 is not essential for viability (1), but reg2 null mutants display reduced rates of both glucose-induced proteolysis of maltose permease and inactivation of maltose transport (2), as well as reduced expression of PIS1 and INO1 during growth on glucose (6). reg1 reg2 double null mutants exhibit a severe growth defect as compared to either wild type or reg1 null mutants (1).

Overexpression of REG2 complements the slow-growth defect of a reg1 mutant (1), but does not complement defects in glycogen accumulation or glucose repression displayed by reg1 nulls (1). Overexpression of REG2 in a reg1 null mutant does restore the glucose-induced proteolysis of maltose permease and partially reinstates the inactivated maltose transport, but does not affect the insensitivity of MAL gene expression to repression by glucose (2).

Last updated: 2005-10-05