Rescue of mitochondrial import failure by intercellular organellar transfer

Hope I. Needs, Emily Glover, Gonçalo C. Pereira, Alina Witt, Wolfgang Hübner, Mark P. Dodding, Jeremy M. Henley () and Ian Collinson ()
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Hope I. Needs: University of Bristol
Emily Glover: University of Bristol
Gonçalo C. Pereira: University of Bristol
Alina Witt: Universität Bielefeld
Wolfgang Hübner: Universität Bielefeld
Mark P. Dodding: University of Bristol
Jeremy M. Henley: University of Bristol
Ian Collinson: University of Bristol

Nature Communications, 2024, vol. 15, issue 1, 1-17

Abstract: 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 cell’s energy supplies – particularly troublesome for energy-demanding cells of nervous tissue and muscle. Unsurprisingly then, import breakdown is implicated in disease. Here, we explore the consequences of import failure in mammalian cells; wherein, blocking the import machinery impacts mitochondrial ultra-structure and dynamics, but, surprisingly, does not affect import. Our data are consistent with a response involving intercellular mitochondrial transport via tunnelling nanotubes to import healthy mitochondria and jettison those with blocked import sites. These observations support the existence of a widespread mechanism for the rescue of mitochondrial dysfunction.

Date: 2024
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DOI: 10.1038/s41467-024-45283-2

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