Journal article
Identification of a Protein Mediating Respiratory Supercomplex Stability
Cell metabolism, Vol.15(3), pp.348-360
03/07/2012
DOI: 10.1016/j.cmet.2012.02.006
PMCID: PMC3302151
PMID: 22405070
Abstract
The complexes of the electron transport chain associate into large macromolecular assemblies, which are believed to facilitate efficient electron flow. We have identified a conserved mitochondrial protein, named respiratory supercomplex factor 1 (Rcf1—Yml030w), that is required for the normal assembly of respiratory supercomplexes. We demonstrate that Rcf1 stably and independently associates with both Complex III and Complex IV of the electron transport chain. Deletion of the RCF1 gene caused impaired respiration, probably as a result of destabilization of respiratory supercomplexes. Consistent with the hypothetical function of these respiratory assemblies, loss of RCF1 caused elevated mitochondrial oxidative stress and damage. Finally, we show that knockdown of HIG2A, a mammalian homolog of RCF1, causes impaired supercomplex formation. We suggest that Rcf1 is a member of an evolutionarily conserved protein family that acts to promote respiratory supercomplex assembly and activity.
► Electron transport chain complexes associate into respiratory supercomplexes ► Pan-eukaryotic inner membrane protein Rcf1 binds Complexes III and IV independently ► Rcf1 is required for normal supercomplex organization in yeast and mammals ► Loss of Rcf1 causes increased oxidative damage
Details
- Title: Subtitle
- Identification of a Protein Mediating Respiratory Supercomplex Stability
- Creators
- Yu-Chan Chen - Department of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT 84112, USAEric B Taylor - Department of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT 84112, USANoah Dephoure - Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USAJin-Mi Heo - Department of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT 84112, USAAline Tonhato - Department of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT 84112, USAIoanna Papandreou - Division of Radiation and Cancer Biology, Department of Radiation Oncology at Stanford University School of Medicine, Stanford, CA 94305, USANandita Nath - Division of Radiation and Cancer Biology, Department of Radiation Oncology at Stanford University School of Medicine, Stanford, CA 94305, USANicolas C Denko - Division of Radiation and Cancer Biology, Department of Radiation Oncology at Stanford University School of Medicine, Stanford, CA 94305, USASteven P Gygi - Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USAJared Rutter - Department of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT 84112, USA
- Resource Type
- Journal article
- Publication Details
- Cell metabolism, Vol.15(3), pp.348-360
- Publisher
- Elsevier Inc
- DOI
- 10.1016/j.cmet.2012.02.006
- PMID
- 22405070
- PMCID
- PMC3302151
- ISSN
- 1550-4131
- eISSN
- 1932-7420
- Language
- English
- Date published
- 03/07/2012
- Academic Unit
- Molecular Physiology and Biophysics
- Record Identifier
- 9984025566702771
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