Selective retention of dysfunctional mitochondria during asymmetric cell division in yeast.

IF 7.8 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
PLoS Biology Pub Date : 2023-09-18 eCollection Date: 2023-09-01 DOI:10.1371/journal.pbio.3002310
Xenia Chelius, Veronika Bartosch, Nathalie Rausch, Magdalena Haubner, Jana Schramm, Ralf J Braun, Till Klecker, Benedikt Westermann
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引用次数: 0

Abstract

Decline of mitochondrial function is a hallmark of cellular aging. To counteract this process, some cells inherit mitochondria asymmetrically to rejuvenate daughter cells. The molecular mechanisms that control this process are poorly understood. Here, we made use of matrix-targeted D-amino acid oxidase (Su9-DAO) to selectively trigger oxidative damage in yeast mitochondria. We observed that dysfunctional mitochondria become fusion-incompetent and immotile. Lack of bud-directed movements is caused by defective recruitment of the myosin motor, Myo2. Intriguingly, intact mitochondria that are present in the same cell continue to move into the bud, establishing that quality control occurs directly at the level of the organelle in the mother. The selection of healthy organelles for inheritance no longer works in the absence of the mitochondrial Myo2 adapter protein Mmr1. Together, our data suggest a mechanism in which the combination of blocked fusion and loss of motor protein ensures that damaged mitochondria are retained in the mother cell to ensure rejuvenation of the bud.

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酵母不对称细胞分裂过程中功能失调线粒体的选择性保留。
线粒体功能下降是细胞衰老的标志。为了抵消这一过程,一些细胞不对称地继承线粒体,使子细胞恢复活力。控制这一过程的分子机制尚不清楚。在这里,我们利用基质靶向D-氨基酸氧化酶(Su9-DAO)选择性触发酵母线粒体的氧化损伤。我们观察到功能失调的线粒体变得融合无能和不稳定。缺乏芽定向运动是由肌球蛋白运动Myo2的募集缺陷引起的。有趣的是,存在于同一细胞中的完整线粒体继续进入芽中,从而确定质量控制直接发生在母亲细胞器的水平上。在缺乏线粒体Myo2衔接蛋白Mmr1的情况下,选择健康细胞器进行遗传不再有效。总之,我们的数据表明了一种机制,在这种机制中,融合受阻和运动蛋白损失的结合确保了受损的线粒体保留在母细胞中,以确保芽的再生。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
PLoS Biology
PLoS Biology 生物-生化与分子生物学
CiteScore
14.40
自引率
2.00%
发文量
359
审稿时长
3 months
期刊介绍: PLOS Biology is an open-access, peer-reviewed general biology journal published by PLOS, a nonprofit organization of scientists and physicians dedicated to making the world's scientific and medical literature freely accessible. The journal publishes new articles online weekly, with issues compiled and published monthly. ISSN Numbers: eISSN: 1545-7885 ISSN: 1544-9173
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