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Fusion fission and transport control asymmetric inheritance of mitochondria and protein aggregates

机译:融合裂变和运输控制线粒体和蛋白质聚集体的不对称遗传

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摘要

Partitioning of cell organelles and cytoplasmic components determines the fate of daughter cells upon asymmetric division. We studied the role of mitochondria in this process using budding yeast as a model. Anterograde mitochondrial transport is mediated by the myosin motor, Myo2. A genetic screen revealed an unexpected interaction of MYO2 and genes required for mitochondrial fusion. Genetic analyses, live-cell microscopy, and simulations in silico showed that fused mitochondria become critical for inheritance and transport across the bud neck in myo2 mutants. Similarly, fused mitochondria are essential for retention in the mother when bud-directed transport is enforced. Inheritance of a less than critical mitochondrial quantity causes a severe decline of replicative life span of daughter cells. Myo2-dependent mitochondrial distribution also is critical for the capture of heat stress–induced cytosolic protein aggregates and their retention in the mother cell. Together, these data suggest that coordination of mitochondrial transport, fusion, and fission is critical for asymmetric division and rejuvenation of daughter cells.
机译:细胞器和细胞质成分的分配决定了不对称分裂后子代细胞的命运。我们使用出芽酵母作为模型研究了线粒体在此过程中的作用。顺行线粒体运输是由肌球蛋白电机Myo2介导的。遗传筛选显示出MYO2和线粒体融合所需基因的意外相互作用。遗传分析,活细胞显微镜检查和计算机模拟显示融合的线粒体对于myo2突变体的遗传和跨芽颈的运输至关重要。同样,当强制进行芽定向运输时,融合的线粒体对于保留在母亲体内至关重要。少于临界线粒体数量的遗传会导致子代细胞复制寿命的严重下降。依赖于肌2的线粒体分布对于捕获热应激诱导的胞质蛋白聚集及其在母细胞中的保留也至关重要。在一起,这些数据表明线粒体运输,融合和裂变的协调对于子细胞的不对称分裂和复兴至关重要。

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