Evidence of Antagonistic Regulation of Restart from G1 Delay in Response to Osmotic Stress by the Hog1 and Whi3 in Budding Yeast

Hog1 of Saccharomyces cerevisiae is activated by hyperosmotic stress, and this leads to cell-cycle delay in G 1 , but the mechanism by which cells restart from G 1 delay remains elusive. We found that Whi3, a negative regulator of G 1 cyclin, counteracted Hog1 in the restart from G 1 delay caused by...

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Published in:Bioscience, biotechnology, and biochemistry biotechnology, and biochemistry, 2013, Vol.77 (10), p.2002-2007
Main Authors: MIZUNUMA, Masaki, OGAWA, Takafumi, KOYAMA, Tetsuya, SHITAMUKAI, Atsunori, TSUBAKIYAMA, Ryohei, KOMARUYAMA, Tadamasa, YAMAGUCHI, Toshinaga, KUME, Kazunori, HIRATA, Dai
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Language:English
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Summary:Hog1 of Saccharomyces cerevisiae is activated by hyperosmotic stress, and this leads to cell-cycle delay in G 1 , but the mechanism by which cells restart from G 1 delay remains elusive. We found that Whi3, a negative regulator of G 1 cyclin, counteracted Hog1 in the restart from G 1 delay caused by osmotic stress. We have found that phosphorylation of Ser-568 in Whi3 by RAS/cAMP-dependent protein kinase (PKA) plays an inhibitory role in Whi3 function. In this study we found that the phosphomimetic Whi3 S568D mutant, like the Δwhi3 strain, slightly suppressed G 1 delay of Δhog1 cells under osmotic stress conditions, whereas the non-phosphorylatable S568A mutation of Whi3 caused prolonged G 1 arrest of Δhog1 cells. These results indicate that Hog1 activity is required for restart from G 1 arrest under osmotic stress conditions, whereas Whi3 acts as a negative regulator for this restart mechanism.
ISSN:0916-8451
1347-6947
DOI:10.1271/bbb.130260