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Fission yeast pheromone blocks S‐phase by inhibiting the G 1 cyclin B–p34 cdc2 kinase
Author(s) -
Stern Bodo,
Nurse Paul
Publication year - 1997
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/16.3.534
Subject(s) - biology , yeast , schizosaccharomyces , cyclin , cyclin dependent kinase 1 , kinase , cyclin dependent kinase , microbiology and biotechnology , cell cycle , saccharomyces cerevisiae , biochemistry , schizosaccharomyces pombe , genetics , gene
Yeast pheromones block cell cycle progression in G 1 in order to prepare mating partners for conjugation. We have investigated the mechanism underlying pheromone‐induced G 1 arrest in the fission yeast Schizosaccharomyces pombe . We find that the G 1 ‐specific transcription factor p65 cdc10 –p72 res1/sct1 which controls the expression of S‐phase genes is fully activated in pheromone, unlike the analogous control in budding yeast. In contrast, the G 1 function of p34 cdc2 acting after activation of the G 1 ‐specific transcription is blocked. Pheromone inhibits the p34 cdc2 kinase associated with both the G 1 ‐specific B‐type cyclin p45 cig2 and the B‐type cyclin p56 cdc13 and overexpression of p45 cig2 or p47 cdc13Δ90 overcomes the pheromone‐induced G 1 arrest. G 1 arrest is compromised in enlarged cells. We suggest that onset of S‐phase is controlled by pheromone inhibiting the B‐cyclin‐associated kinase in G 1 , and that increasing cell size contributes to the mechanism for pheromone adaptation. Thus, pheromone in fission and budding yeast acts similarly in inhibiting the G 1 cyclin‐dependent kinase (CDK), but differs in its effects on the G 1 /S transcriptional control, suggesting that inhibition of CDKs may be a more general mechanism for the control of G 1 progression compared with G 1 /S transcriptional control.