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

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  • MIZUNUMA Masaki
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
  • OGAWA Takafumi
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
  • KOYAMA Tetsuya
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
  • SHITAMUKAI Atsunori
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
  • TSUBAKIYAMA Ryohei
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
  • KOMARUYAMA Tadamasa
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
  • YAMAGUCHI Toshinaga
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
  • KUME Kazunori
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University
  • HIRATA Dai
    Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University

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タイトル別名
  • Evidence of Antagonistic Regulation of Restart from G<sub>1</sub> Delay in Response to Osmotic Stress by the Hog1 and Whi3 in Budding Yeast

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Hog1 of Saccharomyces cerevisiae is activated by hyperosmotic stress, and this leads to cell-cycle delay in G1, but the mechanism by which cells restart from G1 delay remains elusive. We found that Whi3, a negative regulator of G1 cyclin, counteracted Hog1 in the restart from G1 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 G1 delay of Δhog1 cells under osmotic stress conditions, whereas the non-phosphorylatable S568A mutation of Whi3 caused prolonged G1 arrest of Δhog1 cells. These results indicate that Hog1 activity is required for restart from G1 arrest under osmotic stress conditions, whereas Whi3 acts as a negative regulator for this restart mechanism.

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