| Project/Area Number |
15K14511
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cell biology
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| Research Institution | Kyushu University |
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Principal Investigator |
Fujiki Yukio 九州大学, 生体防御医学研究所, 特任教授 (70261237)
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| Co-Investigator(Renkei-kenkyūsha) |
OKUMOTO KANJI 九州大学, 大学院理学研究院, 助教 (20363319)
HONSHO MASANORI 九州大学, 生体防御医学研究所, 特任准教授 (90372747)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | ペルオキシソーム / カタラーゼ / BAK / VDAC2 / 酸化ストレス / 細胞死抑制 / アポトーシス / ミトコンドリア / オルガネラ形成・形態 / レドックスバランス |
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| Outline of Final Research Achievements |
We found that VDAC2 encoding a mitochondrial porin is a causal gene of a peroxisome-deficient CHO mutant, ZP114 showing the impaired import of peroxisome matrix proteins such as catalase. Loss of VDAC2 leads to localization shift of a proapoptotic factor BAK from mitochondria to peroxisomes, resulting in permeabilization of peroxisomal membrane in a manner similar to mitochondrial outer membrane. A part of BAK potentially localizes to peroxisomes and regulates peroxisome integrity and the release of catalase from peroxisomes to the cytosol in normal cells, which can counteracts with commitment of apoptosis by various oxidative stresses including reactive oxygen species.
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