The SKS1 gene was originally identified as a multicopy suppressor of the growth defect of snf3 null mutations on low glucose concentrations. Snf3p is required for the rapid induction of HXT2 during growth on low substrate concentrations. Loss of Snf3p leads to a dramatic delay in expression of HXT2. Adaptation to low substrate concentrations does not occur in snf3 sks1 double null mutant strains, suggesting that SKS1 is required for the glucose-dependent expression of HXT2 in the absence of Snf3p activity. Over-expression of SKS1 leads to over-expression of Hxt2p, thus explaining the mechanism of suppression of the snf3 defect. SKS1 defines a novel, Snf3p-independent pathway for the expression of Hxt2p. Under certain growth conditions, over-expression of SKS1 itself leads to a growth defect which is diminished in snf3 hxt2 double mutants. This suggests that over-expression of Hxt2p at physiologically inappropriate times is detrimental to the cells.