The [PSI+] prion modulates cytochrome c oxidase deficiency caused by deletion of COX12

Author:

Saini Pawan Kumar1,Dawitz Hannah2,Aufschnaiter Andreas2,Bondarev Stanislav3,Thomas Jinsu1,Amblard Amélie1,Stewart James45,Thierry-Mieg Nicolas1,Ott Martin26,Pierrel Fabien1ORCID

Affiliation:

1. Univ. Grenoble Alpes, CNRS, UMR 5525, VetAgro Sup, Grenoble INP, TIMC, 38000 Grenoble, France

2. Department of Biochemistry and Biophysics, Stockholm University, Stockholm 10691, Sweden

3. Department of Genetics and Biotechnology, St. Petersburg State University, St. Petersburg, Russia

4. Max Planck Institute for Biology of Ageing, Joseph-Stelzmann-Str. 9b, 50931 Cologne, Germany

5. Wellcome Centre for Mitochondrial Research, Biosciences Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, NE2 4HH, United Kingdom

6. Department of Medical Biochemistry and Cell Biology, University of Gothenburg, Gothenburg 40530, Sweden

Abstract

Yeast cells lacking the Cox12 subunit of Cytochrome c (CcO) oxidase are impaired in mitochondrial respiration. With a combination of experimental evolution, genetics, and biochemistry, we prove that elimination of the PSI+ prion improves CcO oxidase activity and respiratory metabolism in strains lacking Cox12.

Publisher

American Society for Cell Biology (ASCB)

Subject

Cell Biology,Molecular Biology

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