Further characterization of a size control gene in Saccharomyces cerevisiae.
The DAF1-1 mutation reduces cell size and reduces or eliminates G1 phase in Saccharomyces cerevisiae, and results in alpha-factor resistance. DAF1-1 cells transferred into low cycloheximide express an increased G1 phase in their cycle, suggesting that G1 regulation is present but cryptic in the DAF1-1 cycle in rich medium. DAF1-1 reduces cell size by the criterion of RNA content per cell as well as cell volume. The alpha-factor resistance of DAF1-1 cannot be suppressed by bypassing the pheromone-receptor interaction with 'signalling-constitutive' mutations, suggesting that pheromone binding and initial signalling is normal in DAF1-1 strains, but that division arrest in response to the signal is specifically defective. Consistent with this idea, the cdc28-13 mutation significantly suppresses DAF1-1 alpha-factor resistance at permissive temperature; CDC28 is a gene required specifically for START and the G1/S transition, and does not affect pheromone response. Genetic results additional to those previously reported confirm that the wild-type dafl+/WHI1 gene is non-essential; this result may be surprising since the gene product is apparently rate-limiting for the G1/S transition: its deletion increases cell size, and multiple copies decrease cell size.
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Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98104.
D000945:Antigens, Differentiation, T-Lymphocyte / Q000235:genetics*; D018106:CD28 Antigens; D005800:Genes, Fungal; D005809:Genes, Regulator; D007399:Interphase; D008938:Mitosis; D009154:Mutation; D012331:RNA, Fungal / Q000032:analysis; D012441:Saccharomyces cerevisiae / Q000166:cytology / Q000235:genetics*; D015398:Signal Transduction
D000945:Antigens, Differentiation, T-Lymphocyte; D018106:CD28 Antigens; D012331:RNA, Fungal