| Project/Area Number |
15K14574
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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 |
Genetics/Chromosome dynamics
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| Research Institution | Nagoya University |
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Principal Investigator |
MORI Ikue 名古屋大学, 理学研究科, 教授 (90219999)
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| Co-Investigator(Renkei-kenkyūsha) |
NAKANO Shunji 名古屋大学, 大学院理学研究科, 助教 (60608529)
TSUKADA Yuki 名古屋大学, 大学院理学研究科, 助教 (80580000)
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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: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 老化 / 活性酸素 / 遺伝学 / 線虫 |
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| Outline of Final Research Achievements |
Reactive oxygen species (ROS) are recognized as important signal molecules regulating various biological processes. Low levels of ROS released from mitochondria extend lifespan. We identified a novel mechanism of ROS-mediated lifespan extension by generating fine-tuned ROS level at the plasma membrane through a peroxidase/dual oxidase system in Caenorhabditis elegans. A redox co-factor, pyrroloquinoline quinone (PQQ), activates dual oxidase (DUOX)/BLI-3 to produce the ROS H2O2 at the plasma membrane, which is subsequently degraded by peroxidase/MLT-7 to generate the appropriate levels of ROS. The ROS signal appeared to be mediated by the oxidative stress transcriptional factors SKN-1/Nrf2 and JUN-1. We propose that low levels of ROS, fine-tuned by the peroxidase/dual oxidase system at the plasma membrane, act as second messengers, to extend lifespan by the effect of hormesis.
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