The role for the intracellular degradation system autophagy in protein synthesis during starvation
| Project/Area Number |
26293060
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General medical chemistry
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Mizushima Noboru 東京大学, 医学(系)研究科(研究院), 教授 (10353434)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥16,120,000 (Direct Cost: ¥12,400,000、Indirect Cost: ¥3,720,000)
Fiscal Year 2016: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2014: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
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| Keywords | オートファジー / 細胞内分解 / タンパク質合成 / 蛋白質 / 細胞・組織 / 遺伝子 |
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| Outline of Final Research Achievements |
Autophagy is a major intracellular degradation system that is strongly induced upon nutrient starvation, but its physiological importance is not well understood. In this study, we tested the possibility that autophagy provides amino acids to produce proteins required for starvation adaptation in vivo. We found that protein synthesis is indeed impaired in autophagy-deficient livers during starvation. Proteomic analysis of livers from wild-type and autophagy-defective liver under normal and starvation conditions revealed that autophagy deficiency caused more drastic changes in proteome profiles than starvation. Furthermore, the intracellular amino acids levels were not significantly changed in autophagy-deficient livers even under starvation condition. These data suggest that translation attenuation in autophagy-deficient livers is caused not due to a lack of amino acids provided by autophagy but to a defect in liver homeostasis.
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Report
(4 results)
Research Products
(32 results)
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[Journal Article] Dynamic involvement of ATG5 in cellular stress responses.2014
Author(s)
Lin, H.H., Lin, S.M., Chung, Y., Vonderfecht, S., Camden, J.M., Flodby, P., Borok, Z., Limesand, K.H., Mizushima, N., Ann, D.K
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Journal Title
Cell Death Dis.
Volume: 5
Issue: 10
Pages: 1-12
DOI
Related Report
Peer Reviewed
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