G(1) CYCLIN TURNOVER AND NUTRIENT-UPTAKE ARE CONTROLLED BY A COMMON PATHWAY IN YEAST

Entry into a new cell cycle is triggered by environmental signals at a point called Start in G(1) phase. A key regulator of this transition step in yeast is the CDC28 kinase together with its short-lived regulatory subunits called G(1)-cyclins or CLN proteins. To identify genes involved in G(1)-cyclin degradation, we employed a genetic screen by selecting for stable CLN1-beta-galactosidase fusion proteins. Surprisingly, one group of mutants was found to be allelic to GRR1, a gene previously described to be involved in glucose uptake, glucose repression, and divalent cation transport. In grr1 mutants, both CLN1 and CLN2 cyclins are significantly stabilized. A suppressor analysis indicated that G(1)-cyclin stabilization in grr1 was not a consequence of the nutrient uptake defect. This suggests that the GRR1 gene product is part of a common regulatory pathway linking two functions important for cell growth, nutrient uptake, and G(1) cyclin-controlled cell division.