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Control of Swe1p degradation by the morphogenesis checkpoint
Author(s) -
Sia Rey A.L.,
Bardes Elaine S.G.,
Lew Daniel J.
Publication year - 1998
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/17.22.6678
Subject(s) - biology , morphogenesis , degradation (telecommunications) , microbiology and biotechnology , genetics , gene , computer science , telecommunications
In the budding yeast Saccharomyces cerevisiae , a cell cycle checkpoint coordinates mitosis with bud formation. Perturbations that transiently depolarize the actin cytoskeleton cause delays in bud formation, and a ‘morphogenesis checkpoint’ detects the actin perturbation and imposes a G 2 delay through inhibition of the cyclin‐dependent kinase, Cdc28p. The tyrosine kinase Swe1p, homologous to wee1 in fission yeast, is required for the checkpoint‐mediated G 2 delay. In this report, we show that Swe1p stability is regulated both during the normal cell cycle and in response to the checkpoint. Swe1p is stable during G 1 and accumulates to a peak at the end of S phase or in early G 2 , when it becomes unstable and is degraded rapidly. Destabilization of Swe1p in G 2 and M phase depends on the activity of Cdc28p in complexes with B‐type cyclins. Several different perturbations of actin organization all prevent Swe1p degradation, leading to the persistence or further accumulation of Swe1p, and cell cycle delay in G 2 .

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