The Rho-GAP Bem2p plays a GAP-independent role in the morphogenesis
checkpoint.
Aron Marquitz (1), Jacob Harrison (1), Indrani Bose (1), Daniel
Lew (1)
(1) Department of Pharmacology and Cancer Biology, Duke University
Medical Center, Durham, NC 27710, USA
In the budding yeast Saccharomyces cerevisiae the morphogenesis
checkpoint delays mitosis in response to environmental perturbations
that delay bud formation. The mitotic delay is due to inhibitory
phosphorylation of the cyclin dependent kinase Cdc28p by the tyrosine
kinase Swe1p. This involves both the accumulation of Swe1p itself and
the activation of a second pathway involving the mitogen-activated
protein kinase (MAPK) homolog, Mpk1p/Slt2p. We now show that cells
lacking Bem2p do not delay mitosis when bud formation is blocked and are
therefore defective in some aspect of the morphogenesis checkpoint.
Bem2p is a Rho GTPase activating protein (GAP). However, cells
containing catalytically inactive Bem2p display an intact morphogenesis
checkpoint, suggesting that the role of Bem2p in the checkpoint is
distinct from its role as a Rho GAP. Surprisingly, Swe1p accumulation
and Mpk1p/Slt2p activation both occur normally in cells lacking BEM2,
but these cells are nevertheless unable to promote the inhibitory Cdc28p
phosphorylation that is required for proper checkpoint function.
Therefore, Bem2p appears to define a novel pathway in the morphogenesis
checkpoint.
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