Mutants isolated in this screen grow slowly and are noticeably enlarged compared to wild type cells. We have further characterized one of these mutants. Although induction of CLN3 mRNA levels by glucose is blocked in this mutant, increases in other messages modulated by glucose remain normal. The mutation does not block ectopic expression of CLN3 from the CUP1 promoter, and this expression of CLN3 at least partially cures the size defect in these mutants. We have used complementation of the slow growth phenotype to clone the wild type copy of the gene affected by this mutation from a yeast genomic library.
Efforts are currently underway to identify the cloned gene.