ArticleNature communications2020
Mitochondrial peptide BRAWNIN is essential for vertebrate respiratory complex III assembly.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 146 citations in OpenAlex.
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- MENTSH: A novel mitochondrial microprotein linked to a SNP associated with type 2 diabetes.Theranostics · 2026Article
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- Mammalian mitohormesis: from mitochondrial stressors to organismal benefits.The EMBO journal · 2025Review
- Mitochondrial Microproteins: Emerging Regulators in Neurodevelopment and Neurodegeneration.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
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- Cellular function of the GndA microprotein during heat shock.bioRxiv : the preprint server for biology · 2025Article
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- Proteogenomics Reveals Microproteins in Activated T Cells.Molecular & cellular proteomics : MCP · 2025Article
- Eukaryotic Microproteins.Annual review of biochemistry · 2025Review
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
27 authors at 6 institutions in 4 countries.
Funding
Abstract
The emergence of small open reading frame (sORF)-encoded peptides (SEPs) is rapidly expanding the known proteome at the lower end of the size distribution. Here, we show that the mitochondrial proteome, particularly the respiratory chain, is enriched for small proteins. Using a prediction and validation pipeline for SEPs, we report the discovery of 16 endogenous nuclear encoded, mitochondrial-localized SEPs (mito-SEPs). Through functional prediction, proteomics, metabolomics and metabolic flux modeling, we demonstrate that BRAWNIN, a 71 a.a. peptide encoded by C12orf73, is essential for respiratory chain complex III (CIII) assembly. In human cells, BRAWNIN is induced by the energy-sensing AMPK pathway, and its depletion impairs mitochondrial ATP production. In zebrafish, Brawnin deletion causes complete CIII loss, resulting in severe growth retardation, lactic acidosis and early death. Our findings demonstrate that BRAWNIN is essential for vertebrate oxidative phosphorylation. We propose that mito-SEPs are an untapped resource for essential regulators of oxidative metabolism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.