Regulation of mitochondrial function in the mutations of the GSP1 gene encoding nuclear small G protein.
| Project/Area Number |
18K11084
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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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| Review Section |
Basic Section 59040:Nutrition science and health science-related
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| Research Institution | Kanazawa Gakuin University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 核内低分子量Gタンパク質 / グリセロール代謝 / マイトファジー / MAPキナーゼ / AMPK / 浸透圧ストレス / グルコース抑制 / 出芽酵母 / ミトコンドリア / 酵母 / 低分子量Gタンパク質 / サイレンシング |
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| Outline of Final Research Achievements |
The ras-like nuclear small G protein, Ran, functions in nuclear-cytosolic transport and regulatory signal transmission. Growth deficiency, due to mutations in the GSP1 gene, which encodes Ran, was allele specific. Specifically, the gsp1-1894 cells lost mitochondria, and could not grow on media containing glycerol, galactose or maltose. Growth deficiency on galactose medium was further suppressed by high dosage of the SIP2 DNA, which encodes the cytosolic beta-subunit of AMPK. This suggests that higher cytosolic activity of AMPK is required for the utilization of an alternative carbon source in gsp1-1894 cells.
The gsp1-1894 cells grew better on a high salt medium (1 M NaCl), and had increased expression levels of GPD1-lacZ. Furthermore, disruption of the HOG1 gene suppressed their growth deficiency on glycerol medium. These findings suggest that altered activation of Hog1 in the gsp1-1894 cells resulted in the loss of mitochondria and inhibition of glycerol metabolism.
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| Academic Significance and Societal Importance of the Research Achievements |
出芽酵母の核内低分子量Gタンパク質遺伝子GSP1で分離した多数の変異の中にグリセロールを炭素源として資化できないものを発見し、この変異細胞中でミトコンドリアそのものの量が減少していることがわかった。この現象にはGSP1の62番目のリジン残基の変化が決定的であった。また、この変異株はグルコース以外の発酵性炭素源でも著しく増殖能が低下しており、酵母AMPKの細胞質内βサブユニットのSIP2遺伝子の大量供給によって増殖能低下表現型が回復した。本研究を通し核内低分子量Gタンパク質遺伝子GSP1によってミトコンドリア機能とグルコース抑制能が調節されていることが強く示唆された。
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Report
(4 results)
Research Products
(3 results)
