Mitochondria‐type GPAT is required for mitochondrial fusion
書誌事項
- 公開日
- 2013-04-09
- 資源種別
- journal article
- 権利情報
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- https://www.springernature.com/gp/researchers/text-and-data-mining
- https://www.springernature.com/gp/researchers/text-and-data-mining
- DOI
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- 10.1038/emboj.2013.77
- 公開者
- Springer Science and Business Media LLC
この論文をさがす
説明
Glycerol-3-phosphate acyltransferase (GPAT) is involved in the first step in glycerolipid synthesis and is localized in both the endoplasmic reticulum (ER) and mitochondria. To clarify the functional differences between ER-GPAT and mitochondrial (Mt)-GPAT, we generated both GPAT mutants in C. elegans and demonstrated that Mt-GPAT is essential for mitochondrial fusion. Mutation of Mt-GPAT caused excessive mitochondrial fragmentation. The defect was rescued by injection of lysophosphatidic acid (LPA), a direct product of GPAT, and by inhibition of LPA acyltransferase, both of which lead to accumulation of LPA in the cells. Mitochondrial fragmentation in Mt-GPAT mutants was also rescued by inhibition of mitochondrial fission protein DRP-1 and by overexpression of mitochondrial fusion protein FZO-1/mitofusin, suggesting that the fusion/fission balance is affected by Mt-GPAT depletion. Mitochondrial fragmentation was also observed in Mt-GPAT-depleted HeLa cells. A mitochondrial fusion assay using HeLa cells revealed that Mt-GPAT depletion impaired mitochondrial fusion process. We postulate from these results that LPA produced by Mt-GPAT functions not only as a precursor for glycerolipid synthesis but also as an essential factor of mitochondrial fusion.
収録刊行物
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- The EMBO Journal
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The EMBO Journal 32 (9), 1265-1279, 2013-04-09
Springer Science and Business Media LLC
