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2021 Fiscal Year Final Research Report

Investigation of the basic principle of organelle-mass homeostasis

Research Project

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Project/Area Number 19K06662
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 44010:Cell biology-related
Research InstitutionKyushu University

Principal Investigator

Yanagitani Kota  九州大学, 生体防御医学研究所, 准教授 (70614775)

Project Period (FY) 2019-04-01 – 2022-03-31
Keywordsオルガネラ / ミトコンドリア / 翻訳制御
Outline of Final Research Achievements

If one would investigate a homeostasis, having methods to disturb it are important. Therefore, in this study, we established cells that can artificially decrease the amount of a targeted organelle, then, investigated the cellular responses against the deficiency of the organelle. Using transcriptomics, proteomics, and live cell imaging, we uncovered that Integrated Stress Response (ISR) was found to be activated under the mitochondrial deficiency. Under ISR, protein synthesis in the mitochondria is intact, whereas that in the cytosol is attenuated. Given that respiratory chain complexes are chimera between mitochondrially synthesized proteins and cytosolic synthesized proteins, balanced synthesis of the two group proteins is important. Under ISR, only cytosolic protein synthesis is suppressed, indicating that a balance regulation of mitochondria-cytosol protein synthesis occurs under mitochondrial deficiency.

Free Research Field

細胞生物学

Academic Significance and Societal Importance of the Research Achievements

ミトコンドリア量の異常減少は、ガンや糖尿病、脳卒中などの疾患や老化の過程で起こることが知られている。本研究では、ミトコンドリア不足の状態は、ISRを活性化させ、ミトコンドリア-サイトゾルタンパク質合成のアンバランスを解消させることが明らかになった。ただし、長く続くISRの活性化は、細胞死の誘導や拒食症誘導ホルモンGDF15の放出などを介して、細胞・個体レベルでの悪影響を引き起こすことが知られている。そのため、ミトコンドリア不足の可能性がある上記の疾患群では、ISRの亢進による病態悪化が起こっているかもしれない。本研究成果は、上記疾患群のISRを対象とした治療法の開発に貢献する可能性がある。

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Published: 2023-01-30  

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