The novel mechanism of avoidance of ER stress in yeast
| Project/Area Number |
25892018
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Applied microbiology
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| Research Institution | Nara Institute of Science and Technology |
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Principal Investigator |
KIMATA Yuki 奈良先端科学技術大学院大学, バイオサイエンス研究科, 研究員 (10706261)
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| Project Period (FY) |
2013-08-30 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 小胞体ストレス応答 / Ire1 / 出芽酵母 |
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| Outline of Final Research Achievements |
Eukaryotic cells cumulatively evoke the endoplasmic reticulum (ER)-stress response or the unfolded protein response (UPR). Cellular stress causing the UPR has been believed to accompany accumulation of unfolded proteins in the ER. In consistent to this idea, ER stress sensors including the ER-located type-I transmembrane protein Ire1 is activated through ER accumulation of unfolded proteins. However, recent studies revealed that membrane-lipid abnormalities and/or disturbance of intracellular respiration also cause ER stress which initiates the UPR. In the present study, I have addressed modulation of Ire1’s activity by mitochondrial dysfunction in yeast Saccharomyces cerevisiae cells. Namely, Ire1 gets insensitive to weak ER stress in cells lacking normal mitochondrial function.
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Report
(3 results)
Research Products
(8 results)
