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The Rho‐GAP Bem2p plays a GAP‐independent role in the morphogenesis checkpoint
Author(s) -
Marquitz Aron R.,
Harrison Jacob C.,
Bose Indrani,
Zyla Trevin R.,
McMillan John N.,
Lew Daniel J.
Publication year - 2002
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/cdf416
Subject(s) - microbiology and biotechnology , cell polarity , morphogenesis , biology , g2 m dna damage checkpoint , cyclin dependent kinase 1 , cell cycle checkpoint , mitosis , polarity (international relations) , cell cycle , cell , genetics , gene
The Saccharomyces cerevisiae morphogenesis checkpoint delays mitosis in response to insults that impair actin organization and/or bud formation. The delay is due to accumulation of the inhibitory kinase Swe1p, which phosphorylates the cyclin‐dependent kinase Cdc28p. Having screened through a panel of yeast mutants with defects in cell morphogenesis, we report here that the polarity establishment protein Bem2p is required for the checkpoint response. Bem2p is a Rho‐GTPase activating protein (GAP) previously shown to act on Rho1p, and we now show that it also acts on Cdc42p, the GTPase primarily responsible for establishment of cell polarity in yeast. Whereas the morphogenesis role of Bem2p required GAP activity, the checkpoint role of Bem2p did not. Instead, this function required an N‐terminal Bem2p domain. Thus, this single protein has a GAP‐dependent role in promoting cell polarity and a GAP‐independent role in responding to defects in cell polarity by enacting the checkpoint. Surprisingly, Swe1p accumulation occurred normally in bem2 cells, but they were nevertheless unable to promote Cdc28p phosphorylation. Therefore, Bem2p defines a novel pathway in the morphogenesis checkpoint.