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bioRxiv · 10.1101/2022.11.30.518494

Intercellular Mitochondrial Transfer as a Rescue Mechanism in Response to Protein Import Failure

Needs, H. I.·Pereira, G. C.·Glover, E.·Hubner, W.·Henley, J.·Collinson, I.
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Abstract

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 cells 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 transfer via tunnelling 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).

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Needs, H. I., Pereira, G. C., Glover, E., Hubner, W., Henley, J., Collinson, I.. 2022-12-01. Intercellular Mitochondrial Transfer as a Rescue Mechanism in Response to Protein Import Failure. https://doi.org/10.1101/2022.11.30.518494

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