Intercellular Mitochondrial Transfer as a Rescue Mechanism in Response to Protein Import Failure
Intercellular Mitochondrial Transfer as a Rescue Mechanism in Response to Protein Import Failure
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细胞间线粒体转移作为应对蛋白质导入失败的救援机制
DOI：
10.1101/2022.11.30.518494
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发表时间：
2022
期刊：
影响因子：
--
通讯作者：
Needs H
中科院分区：
文献类型：
--
作者：
Needs H
线粒体是真核细胞的发电站，主要由从细胞质输入的核编码蛋白质组成。因此，输入机制的问题将破坏它们的再生能力和细胞的能量（ATP）代谢，特别是对需要能量的细胞，如神经元和肌细胞。因此，不正常的输入与疾病有关，这并不奇怪。这项研究探讨了哺乳动物细胞中输入失败的后果;其中，阻断输入机制对线粒体超微结构和动力学具有深远的影响，但令人惊讶的是，不影响输入。对此的解释是一个令人惊讶的反应，涉及细胞间线粒体的转移和隧道纳米管：用于输入健康的线粒体和丢弃那些堵塞的输入位点。这些观察结果支持存在一个广泛的机制，为拯救线粒体蛋白输入fault.One-Sentence SummaryA线粒体进口救援机制，涉及细胞间线粒体运输通过隧道纳米管（TNT）。
Mitochondria are the powerhouses of eukaryotic cells, composed mostly of nuclear-encoded proteins imported from the cytosol. Thus, problems with the import machinery will disrupt their regenerative capacity and the cell’s energy (ATP) supplies–particularly troublesome for energy demanding cells like neurons and myocytes. Unsurprisingly then, dysfunctional import is implicated in disease. This study explores the consequences of import failure in mammalian cells; wherein, blocking the import machinery has profound effects on mitochondrial ultra-structure and dynamics, but, surprisingly, does not impact import. The explanation is an astonishing response involving intercellular mitochondrial transferviatunnelling nanotubes: for the import of healthy mitochondria and jettisoning of those with jammed import sites. These observations support the existence of a widespread mechanism for the rescue of mitochondrial protein import failure.One-Sentence SummaryA mitochondrial import rescue mechanism involving intercellular mitochondrial transport through tunneling nanotubes (TNTs).