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  The [PSI+] prion and HSP104 modulate cytochrome c oxidase deficiency caused by deletion of COX12

Saini, P. K., Dawitz, H., Aufschnaiter, A., Thomas, J., Amblard, A., Stewart, J., et al. (2021). The [PSI+] prion and HSP104 modulate cytochrome c oxidase deficiency caused by deletion of COX12. bioRxiv, 2021.10.08.463630. doi:10.1101/2021.10.08.463630.

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Saini, P. K., Author
Dawitz, H., Author
Aufschnaiter, A., Author
Thomas, J., Author
Amblard, A., Author
Stewart, J.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 Δcox12 strain for ~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 Δcox12 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.Competing Interest StatementThe authors have declared no competing interest.

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 Dates: 2021-10-082021
 Publication Status: Issued
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 Identifiers: DOI: 10.1101/2021.10.08.463630
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Title: bioRxiv
Source Genre: Journal
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Pages: - Volume / Issue: - Sequence Number: - Start / End Page: 2021.10.08.463630 Identifier: -