Listeria monocytogenes exploits the MICOS complex subunit Mic10 to promote mitochondrial fragmentation and cellular infection - Institut Pasteur Access content directly
Preprints, Working Papers, ... Year : 2019

Listeria monocytogenes exploits the MICOS complex subunit Mic10 to promote mitochondrial fragmentation and cellular infection

Abstract

Mitochondrial function adapts to cellular demands and is affected by the ability of the organelle to undergo fusion and fission in response to physiological and non-physiological cues. We previously showed that infection with the human bacterial pathogen Listeria monocytogenes elicits dramatic mitochondrial fission and causes a decrease in the mitochondrial membrane potential. Using quantitative proteomics of purified mitochondria, we searched for host factors involved in L. monocytogenes-induced mitochondrial fission. We found that Mic10, a critical component of the mitochondrial contact site and cristae organizing system (MICOS) complex is significantly enriched in mitochondria isolated from cells infected with wild-type L. monocytogenes, but not with mutant bacteria not expressing the pore-forming toxin listeriolysin O. Increased mitochondrial Mic10 levels did not correlate with upregulated gene transcription, suggesting a post-transcriptional regulatory mechanism. We show that Mic10 is necessary for L. monocytogenes-induced mitochondrial network fragmentation, and that it contributes to L. monocytogenes cellular infection independently of MICOS proteins Mic13, Mic26 and Mic27. Together, L. monocytogenes infection allowed us to uncover a role for Mic10 in mitochondrial fission.
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Dates and versions

pasteur-02389987 , version 1 (02-12-2019)
pasteur-02389987 , version 2 (03-01-2021)

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Attribution - NonCommercial - NoDerivatives

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Filipe Carvalho, Anna Spier, Thibault Chaze, Mariette Matondo, Pascale Cossart, et al.. Listeria monocytogenes exploits the MICOS complex subunit Mic10 to promote mitochondrial fragmentation and cellular infection. 2019. ⟨pasteur-02389987v1⟩

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