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Vol. 12, Issue 1, 53-62, January 2001
*Rice University, Department of Biochemistry and Cell Biology,
Houston Texas 77251; Exposure of yeast cells to an increase in external osmolarity
induces a temporary growth arrest. Recovery from this stress is
mediated by the accumulation of intracellular glycerol and the
transcription of several stress response genes. Increased external
osmolarity causes a transient accumulation of 1N and 2N cells and a
concomitant depletion of S phase cells. Hypertonic stress triggers a
cell cycle delay in G2 phase cells that appears distinct from the
morphogenesis checkpoint, which operates in early S phase cells.
Hypertonic stress causes a decrease in CLB2 mRNA,
phosphorylation of Cdc28p, and inhibition of Clb2p-Cdc28p kinase
activity, whereas Clb2 protein levels are unaffected. Like the
morphogenesis checkpoint, the osmotic stress-induced G2 delay is
dependent upon the kinase Swe1p, but is not tightly correlated with
inhibition of Clb2p-Cdc28p kinase activity. Thus, deletion of
SWE1 does not prevent the hypertonic stress-induced
inhibition of Clb2p-Cdc28p kinase activity. Mutation of the Swe1p
phosphorylation site on Cdc28p (Y19) does not fully eliminate the
Swe1p-dependent cell cycle delay, suggesting that Swe1p may have
functions independent of Cdc28p phosphorylation. Conversely, deletion
of the mitogen-activated protein kinase HOG1 does
prevent Clb2p-Cdc28p inhibition by hypertonic stress, but does not
block Cdc28p phosphorylation or alleviate the cell cycle delay.
However, Hog1p does contribute to proper nuclear segregation after
hypertonic stress in cells that lack Swe1p. These results suggest a
hypertonic stress-induced cell cycle delay in G2 phase that is mediated
in a novel way by Swe1p in cooperation with Hog1p.
Samuel Lunenfeld Research
Institute, Mount Sinai Hospital, Toronto Ontario, Canada M5G 1X5
Lyndon B. Johnson Space
Center-NASA, SD3, Houston, Texas 77058;
§Harvard Medical
School, 240 Longwood Ave., Boston, Massachusetts 02115.
Corresponding author. E-mail address:
gustin{at}bioc.rice.edu.
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