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首页> 外文期刊>BioArchitecture >Imperfect asymmetry: The mechanism governing asymmetric partitioning of damaged cellular components during mitosis
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Imperfect asymmetry: The mechanism governing asymmetric partitioning of damaged cellular components during mitosis

机译：不完美的不对称性：控制有丝分裂期间受损细胞成分不对称分配的机制

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摘要

Aging is universally associated with organism-wide dysfunction and a decline in cellular fitness. From early development onwards, the efficiency of self-repair, energy production, and homeostasis all decrease. Due to the multiplicity of systems that undergo agingrelated decline, the mechanistic basis of organismal aging has been difficult to pinpoint. At the cellular level, however, recent work has provided important insight. Cellular aging is associated with the accumulation of several types of damage, in particular damage to the pro-teome and organelles. Groundbreaking studies have shown that replicative aging is the result of a rejuvenation mechanism that prevents the inheritance of damaged components during division, thereby confining the effects of aging to specific cells, while removing damage from others. Asymmetric inheritance of misfolded and aggregated proteins, as well as reduced mitochondria, has been shown in yeast. Until recendy, however, it was not clear whether a similar mechanism operates in mammalian cells, which were thought to mosdy divide symmetrically. Our group has recendy shown that vimentin establishes mitotic polarity in immortalized mammalian cells, and mediates asymmetric partitioning of multiple factors through directinteraction. These findings prompt a provocative hypothesis: that intermediate filaments serve as asymmetric partitioning modules or "sponges" that, when expressed prior to mitosis, can "clean" emerging cells of the damage they have accumulated.
机译：衰老普遍与整个有机体功能障碍和细胞适应性下降有关。从早期开发开始，自我修复，能源生产和动态平衡的效率都会下降。由于经历衰老相关系统的多样性，很难确定生物衰老的机制基础。但是，在蜂窝级别，最近的工作提供了重要的见识。细胞衰老与几种类型损伤的累积有关，特别是对蛋白质组和细胞器的损伤。突破性研究表明，复制性衰老是复兴机制的结果，该机制可防止分裂过程中受损成分的遗传，从而将衰老的影响限制在特定细胞上，同时消除其他细胞的损害。酵母中显示了错误折叠和聚集的蛋白质的不对称遗传以及线粒体的减少。然而，直到最近，尚不清楚在哺乳动物细胞中是否有类似的机制起作用，而哺乳动物细胞被认为是苔藓对称分裂的。我们的研究小组表明波形蛋白在永生的哺乳动物细胞中建立有丝分裂极性，并通过直接相互作用介导多个因子的不对称分配。这些发现提出了一个令人鼓舞的假设：中间的细丝充当不对称的分隔模块或“海绵”，当在有丝分裂之前表达时，可以“清除”新兴细胞积累的损伤。

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