A nuclear-based quality control pathway for non-imported mitochondrial proteins
Year: 2021
Type: article
Abstract: Mitochondrial import deficiency causes cellular stress due to the accumulation of non-imported mitochondrial precursor proteins. Despite the burden mis-localized mitochondrial precursors place on cells, our understanding of the systems that dispose of these proteins is incomplete. Here, we catalog the location and steady-state abundance of mitochondrial precursor proteins during mitochondrial impairment in S. cerevisiae . We find that a number of non-imported mitochondrial proteins localize to the nucleus, where they are eliminated by proteasome-based nuclear protein quality control. Recognition of mitochondrial precursors by the nuclear quality control machinery requires the presence of an N-terminal mitochondrial targeting sequence (MTS), and impaired breakdown of precursors leads to their buildup in nuclear-associated foci. These results identify the nucleus as a key destination for the disposal of non-imported mitochondrial precursors.
Source: eLife
DOI: 10.7554/elife.61230
Institution: University of Utah
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $2,500
Funders: American Federation for Aging Research, American Heart Association, Glenn Foundation for Medical Research, Kinship Foundation, United Mitochondrial Disease Foundation, Fondation pour la Recherche Médicale, National Institutes of Health, National Institute on Aging, National Institute of General Medical Sciences
OpenAlex ID: W3135984613
