| Budget Amount *help |
¥17,420,000 (Direct Cost: ¥13,400,000、Indirect Cost: ¥4,020,000)
Fiscal Year 2019: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2018: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2017: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
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| Outline of Final Research Achievements |
Mitophagy plays an important role in mitochondrial quality control. We identified that the PP2A (protein phosphatase 2A)-like protein phosphatase Ppg1 was essential for dephosphorylation of mitophagy receptor Atg32 and thus inhibited mitophagy in yeast. We identified the Far complex consisting of Far3-7-8-9-10-11 proteins as Ppg1-binding proteins and Far proteins also essential for dephosphorylation of Atg32. From these findings, we concluded that Ppg1 and the Far complex cooperatively dephosphorylate Atg32 to prevent excessive mitophagy.
Using mammalian culture cells, we found that the anticancer drug gemcitabine induces mitophagy. Notably, the PINK1 and MUL1, but not Parkin have important role in mitophagy induced by gemcitabine. We also identified that Glaucoma-mutant OPTN proteins retain their normal properties as mitophagy receptors, suggesting that mutations in the OPTN gene cause glaucoma through a mechanism independent of mitophagy defects.
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