4.5 Article

Supercomplex-associated Cox26 protein binds to cytochrome c oxidase

Journal

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
Volume 1863, Issue 7, Pages 1643-1652

Publisher

ELSEVIER
DOI: 10.1016/j.bbamcr.2016.04.012

Keywords

Blue native electrophoresis; Cytochrome c oxidase; Protein composition; Respiratory supercomplexes; III-IV supercomplexes; Saccharomyces cerevisiae

Funding

  1. Cluster of Excellence Macromolecular Complexes at the Goethe University Frankfurt (DFG) [EXC 115]
  2. Bundesministerium fur Bildung and Forschung [BMBF 01GM1113B]
  3. National Science Foundation (NSF) [MCB0744067, MCB 1157722]
  4. National Institutes of Health (NIH) [NIH-GM101594]
  5. [SFB815]
  6. Div Of Molecular and Cellular Bioscience
  7. Direct For Biological Sciences [1157722] Funding Source: National Science Foundation

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Here we identified a hydrophobic 6.4 kDa protein, Cox26, as a novel component of yeast mitochondrial supercomplex comprising respiratory complexes III and IV. Multi-dimensional native and denaturing electrophoretic techniques were used to identify proteins interacting with Cox26. The majority of the Cox26 protein was found non-covalently bound to the complex IV moiety of the III-IV supercomplexes. A population of Cox26 was observed to exist in a disulfide bond partnership with the Cox2 subunit of complex IV. No pronounced growth phenotype for Cox26 deficiency was observed, indicating that Cox26 may not play a critical role in the COX enzymology, and we speculate that Cox26 may serve to regulate or support the Cox2 protein. Respiratory supercomplexes are assembled in the absence of the Cox26 protein, however their pattern slightly differs to the wild type III-IV supercomplex appearance. The catalytic activities of complexes III and IV were observed to be normal and respiration was comparable to wild type as long as cells were cultivated under normal growth conditions. Stress conditions, such as elevated temperatures resulted in mild decrease of respiration in non-fermentative media when the Cox26 protein was absent. (C) 2016 Elsevier B.V. All rights reserved.

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