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« Previous AbstractFurther characterization of a size control gene in Saccharomyces cerevisiae    Next Abstract"The DAF2-2 mutation, a dominant inhibitor of the STE4 step in the alpha-factor signaling pathway of Saccharomyces cerevisiae MAT alpha cells" »

Mol Cell Biol


Title:Cell cycle arrest caused by CLN gene deficiency in Saccharomyces cerevisiae resembles START-I arrest and is independent of the mating-pheromone signalling pathway
Author(s):Cross FR;
Address:"Rockefeller University, New York, New York 10021-6399"
Journal Title:Mol Cell Biol
Year:1990
Volume:10
Issue:12
Page Number:6482 - 6490
DOI: 10.1128/mcb.10.12.6482-6490.1990
ISSN/ISBN:0270-7306 (Print) 1098-5549 (Electronic) 0270-7306 (Linking)
Abstract:"Null mutations in three genes encoding cyclin-like proteins (CLN1, CLN2, and CLN3) in Saccharomyces cerevisiae cause cell cycle arrest in G1 (cln arrest). In cln1 cln2 cln3 strains bearing plasmids containing the CLN3 (also called WHI1 or DAF1) coding sequence under the transcriptional control of a galactose-regulated promoter, shift from galactose to glucose medium (shutting off synthesis of CLN3 mRNA) allowed completion of cell cycles in progress but caused arrest in the ensuing unbudded G1 phase. Cell growth was not inhibited in arrested cells. Cell division occurred in glucose medium even if cells were arrested in S phase during the initial 2 h of glucose treatment, suggesting that CLN function may not be required in the cell cycle after S phase. However, when the coding sequence of the hyperactive C-terminal truncation allele CLN3-2 (formerly DAF1-1) was placed under GAL control, cells went through multiple cycles before arresting after a shift from galactose to glucose. These results suggest that the C terminus of the wild-type protein confers functional instability. cln-arrested cells are mating competent. However, cln arrest is distinct from constitutive activation of the mating-factor signalling pathway because cln-arrested cells were dependent on the addition of pheromone both for mating and for induction of an alpha-factor-induced transcript, FUS1, and because MATa/MAT alpha (pheromone-nonresponsive) strains were capable of cln arrest in G1 (although a residual capacity for cell division before arrest was observed in MATa/MAT alpha strains). These results are consistent with a specific CLN requirement for START transit"
Keywords:"Alleles Cell Cycle Cell Division Chromosome Deletion Cyclins/*genetics *Genes, Fungal Kinetics Mating Factor Peptides/*physiology Pheromones/physiology RNA, Messenger/genetics Saccharomyces cerevisiae/cytology/*genetics/growth & development Signal Transdu;"
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. 1990/12/01 Mol Cell Biol. 1990 Dec; 10(12):6482-90. doi: 10.1128/mcb.10.12.6482-6490.1990"

 
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