2015 Fiscal Year Final Research Report
Elucidation of the kinase module to control the endoplasmic reticulum stress response
| Project/Area Number |
25440078
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Cell biology
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | 小胞体ストレス / MAPキナーゼ / AMP活性化キナーゼ |
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| Outline of Final Research Achievements |
Accumulation of unfolded proteins in the lumen of the endoplasmic reticulum (ER) causes ER stress. Snf1, the Saccharomyces cerevisiae ortholog of AMP-activated protein kinase (AMPK), plays a crucial role in the response to various environmental stresses. However, the role of Snf1 in ER stress response remains poorly understood. In this study, we characterize Snf1 as a negative regulator of Hog1 MAPK in ER stress response. The snf1 mutants showed the ER stress resistant phenotype. Activated Hog1 levels were increased by snf1 mutation. Ssk1, a specific activator of MAPKKK functioning upstream of Hog1, was induced by ER stress and its induction was inhibited in a manner dependent on Snf1 activity. Furthermore, we show that the SSK1 promoter is important for Snf1-modulated regulation of Ssk1 expression. Our data suggest that Snf1 downregulates ER stress response signal mediated by Hog1 through negatively regulating expression of its specific activator Ssk1 at the transcriptional level.
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| Free Research Field |
ストレス応答シグナル伝達経路
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