Article

Identification of a protein mediating respiratory supercomplex stability.

Department of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT 84112, USA.
Cell metabolism (impact factor: 17.35). 03/2012; 15(3):348-60. DOI:10.1016/j.cmet.2012.02.006 pp.348-60
Source: PubMed

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.

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Keywords

causes
 
Complex III
 
conserved mitochondrial protein
 
Consistent
 
efficient electron flow
 
electron transport chain
 
electron transport chain associate
 
evolutionarily conserved protein family
 
HIG2A
 
large macromolecular assemblies
 
mitochondrial oxidative stress
 
RCF1
 
RCF1 gene
 
Rcf1 stably
 
respiratory assemblies
 
respiratory supercomplex assembly
 
respiratory supercomplex factor 1
 
respiratory supercomplexes
 

Yu-Chan Chen