Pernice Wolfgang M, Vevea Jason D, Pon Liza A
Department of Pathology and Cell Biology, Columbia University, 630 West 168th Street, P&S 14-442, New York, New York 10032, USA.
Nat Commun. 2016 Feb 3;7:10595. doi: 10.1038/ncomms10595.
Previous studies indicate that replicative lifespan in daughter cells of Sacchraromyces cerevisiae depends on the preferential inheritance of young, high-functioning mitochondria. We report here that mitochondria are functionally segregated even within single mother cells in S. cerevisiae. A high-functioning population of mitochondria accumulates at the tip of the mother cell distal to the bud. We find that the mitochondrial F-box protein (Mfb1p) localizes to mitochondria in the mother tip and is required for mitochondrial anchorage at that site, independent of the previously identified anchorage protein Num1p. Deletion of MFB1 results in loss of the mother-tip-localized mitochondrial population, defects in mitochondrial function and premature replicative ageing. Inhibiting mitochondrial inheritance to buds, by deletion of MMR1, in mfb1Δ cells restores mitochondrial distribution, promotes mitochondrial function and extends replicative lifespan. Our results identify a mechanism that retains a reservoir of high-functioning mitochondria in mother cells and thereby preserves maternal reproductive capacity.
先前的研究表明，酿酒酵母子细胞中的复制寿命取决于年轻、功能良好的线粒体的优先遗传。我们在此报告，即使在酿酒酵母的单个母细胞内，线粒体在功能上也是分离的。一群功能良好的线粒体聚集在母细胞远离芽的一端。我们发现线粒体F-box蛋白（Mfb1p）定位于母细胞尖端的线粒体，并且是该位点线粒体锚定所必需的，这与先前鉴定的锚定蛋白Num1p无关。MFB1的缺失导致母细胞尖端定位的线粒体群体丧失、线粒体功能缺陷和过早的复制衰老。通过缺失MMR1抑制线粒体向芽的遗传，在mfb1Δ细胞中可恢复线粒体分布、促进线粒体功能并延长复制寿命。我们的结果确定了一种机制，该机制在母细胞中保留了一群功能良好的线粒体，从而保持了母体的繁殖能力。
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