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Vol. 10, Issue 10, 3301-3316, October 1999
Center for Molecular Oncology and Department of Molecular Genetics
and Cell Biology, University of Chicago, Chicago, Illinois 60637
Inoculation of diploid budding yeast onto nitrogen-poor agar
media stimulates a MAPK pathway to promote filamentous growth. Characteristics of filamentous cells include a specific pattern of gene
expression, elongated cell shape, polar budding pattern, persistent
attachment to the mother cell, and a distinct cell cycle characterized
by cell size control at G2/M. Although a requirement for MAPK signaling
in filamentous gene expression is well established, the role of this
pathway in the regulation of morphogenesis and the cell cycle remains
obscure. We find that ectopic activation of the MAPK signal pathway
induces a cell cycle shift to G2/M coordinately with other changes
characteristic of filamentous growth. These effects are abrogated by
overexpression of the yeast mitotic cyclins Clb1 and Clb2. In turn,
yeast deficient for Clb2 or carrying cdc28-1N, an allele
of CDK defective for mitotic functions, display enhanced filamentous
differentiation and supersensitivity to the MAPK signal. Importantly,
activation of Swe1-mediated inhibitory phosphorylation of Thr-18 and/or
Tyr-19 of Cdc28 is not required for the MAPK pathway to affect the G2/M
delay. Mutants expressing a nonphosphorylatable mutant Cdc28 or
deficient for Swe1 exhibit low-nitrogen-dependent filamentous growth
and are further induced by an ectopic MAPK signal. We infer that the
MAPK pathway promotes filamentous growth by a novel mechanism that
inhibits mitotic cyclin/CDK complexes and thereby modulates cell shape,
budding pattern, and cell-cell connections.
Corresponding author. E-mail address:
skron{at}midway.uchicago.edu.
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