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J Cell Sci Suppl

Title:		Further characterization of a size control gene in Saccharomyces cerevisiae
Author(s):		Cross FR;
Address:		"Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98104"
Journal Title:		J Cell Sci Suppl
Year:		1989
Volume:		12
Issue:
Page Number:		117 - 127
DOI:		10.1242/jcs.1989.supplement_12.10
ISSN/ISBN:		0269-3518 (Print) 0269-3518 (Linking)
Abstract:		"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"
Keywords:		"Antigens, Differentiation, T-Lymphocyte/*genetics CD28 Antigens *Genes, Fungal Genes, Regulator Interphase Mitosis Mutation RNA, Fungal/analysis Saccharomyces cerevisiae/cytology/*genetics Signal Transduction;"
Notes:		"MedlineCross, F R eng GM26176/GM/NIGMS NIH HHS/ Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. England 1989/01/01 J Cell Sci Suppl. 1989; 12:117-27. doi: 10.1242/jcs.1989.supplement_12.10"