Journal
ELIFE
Volume 8, Issue -, Pages -Publisher
eLIFE SCIENCES PUBL LTD
DOI: 10.7554/eLife.45051
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Funding
- Wellcome [WT106956/Z/15/Z, WT100981/z/13/z]
- European Research Council [249869]
- Medical Research Council
- Oxford University
- Natural Sciences and Engineering Research Council of Canada
- Diabetes UK [11/0004175]
- European Commission
- Royal Society
- BBSRC [BBS/E/T/000PR9819, BBS/E/T/000PR9818, BBS/E/T/000PR5885] Funding Source: UKRI
- MRC [MC_UU_00007/15] Funding Source: UKRI
- European Research Council (ERC) [249869] Funding Source: European Research Council (ERC)
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To generate energy efficiently, the cell is uniquely challenged to co-ordinate the abundance of electron transport chain protein subunits expressed from both nuclear and mitochondrial genomes. How an effective stoichiometry of this many constituent subunits is coordinated post-transcriptionally remains poorly understood. Here we show that Cerox1, an unusually abundant cytoplasmic long noncoding RNA (lncRNA), modulates the levels of mitochondrial complex I subunit transcripts in a manner that requires binding to microRNA-488-3p. Increased abundance of Cerox1 cooperatively elevates complex I subunit protein abundance and enzymatic activity, decreases reactive oxygen species production, and protects against the complex I inhibitor rotenone. Cerox1 function is conserved across placental mammals: human and mouse orthologues effectively modulate complex I enzymatic activity in mouse and human cells, respectively. Cerox1 is the first lncRNA demonstrated, to our knowledge, to regulate mitochondrial oxidative phosphorylation and, with miR-488-3p, represent novel targets for the modulation of complex I activity.
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