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

Saini, P. K., Dawitz, H., Aufschnaiter, A., Bondarev, S., Thomas, J., Amblard, A., et al. (2022). The [PSI+] prion modulates cytochrome c oxidase deficiency caused by deletion of COX12. Mol Biol Cell, mbcE21100499. doi:10.1091/mbc.E21-10-0499.

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Saini, P. K., Author
Dawitz, H., Author
Aufschnaiter, A., Author
Bondarev, S., Author
Thomas, J., Author
Amblard, A., Author
Stewart, J. B.1, Author           
Thierry-Mieg, N., Author
Ott, M., Author
Pierrel, F., Author
Affiliations:
1Stewart – Mitochondrial Mutations and Genome Co-evolution, Research Groups, Max Planck Institute for Biology of Ageing, Max Planck Society, ou_1942301              

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 Abstract: Cytochrome c oxidase is a pivotal enzyme of the mitochondrial respiratory chain, which sustains bioenergetics of eukaryotic cells. Cox12, a peripheral subunit of cytochrome c oxidase, is required for full activity of the enzyme, but its exact function is unknown. Here, experimental evolution of a Saccharomyces cerevisiae Deltacox12 strain for approximately 300 generations allowed to restore the activity of cytochrome c oxidase. In one population, the enhanced bioenergetics was caused by a A375V mutation in the AAA+ disaggregase Hsp104. Deletion or overexpression of HSP104 also increased respiration of the Deltacox12 ancestor strain. This beneficial effect of Hsp104 was related to the loss of the [PSI(+)] prion, which forms cytosolic amyloid aggregates of the Sup35 protein. Overall, our data demonstrate that cytosolic aggregation of a prion impairs the mitochondrial metabolism of cells defective for Cox12. These findings identify a new functional connection between cytosolic proteostasis and biogenesis of the mitochondrial respiratory chain.

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 Dates: 2022-09-212022-12-01
 Publication Status: Issued
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 Identifiers: Other: 36129767
DOI: 10.1091/mbc.E21-10-0499
ISSN: 1939-4586 (Electronic)1059-1524 (Linking)
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Title: Mol Biol Cell
Source Genre: Journal
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