Methylation of ESCRT-III components regulates the timing of cytokinetic abscission

Aurélie Richard, Jérémy Berthelet, Delphine Judith, Tamara Advedissian, Javier Espadas, Guillaume Jannot, Angélique Amo, Damarys Loew, Berangere Lombard, Alexandre G. Casanova, Nicolas Reynoird, Aurélien Roux, Clarisse Berlioz-Torrent, Arnaud Echard, Jonathan B. Weitzman and Souhila Medjkane ()
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Aurélie Richard: UMR7126 Epigenetics and Cell Fate
Jérémy Berthelet: UMR7126 Epigenetics and Cell Fate
Delphine Judith: Institut Cochin
Tamara Advedissian: Institut Pasteur, Université Paris Cité, CNRS UMR3691, Membrane Traffic and Cell Division Unit
Javier Espadas: University of Geneva
Guillaume Jannot: UMR7126 Epigenetics and Cell Fate
Angélique Amo: UMR7126 Epigenetics and Cell Fate
Damarys Loew: PSL Research University, Centre de Recherche, CurieCoreTech Mass Spectrometry Proteomics
Berangere Lombard: PSL Research University, Centre de Recherche, CurieCoreTech Mass Spectrometry Proteomics
Alexandre G. Casanova: Institute for Advanced Biosciences
Nicolas Reynoird: Institute for Advanced Biosciences
Aurélien Roux: University of Geneva
Clarisse Berlioz-Torrent: Institut Cochin
Arnaud Echard: Institut Pasteur, Université Paris Cité, CNRS UMR3691, Membrane Traffic and Cell Division Unit
Jonathan B. Weitzman: UMR7126 Epigenetics and Cell Fate
Souhila Medjkane: UMR7126 Epigenetics and Cell Fate

Nature Communications, 2024, vol. 15, issue 1, 1-17

Abstract: Abstract Abscission is the final stage of cytokinesis, which cleaves the intercellular bridge (ICB) connecting two daughter cells. Abscission requires tight control of the recruitment and polymerization of the Endosomal Protein Complex Required for Transport-III (ESCRT-III) components. We explore the role of post-translational modifications in regulating ESCRT dynamics. We discover that SMYD2 methylates the lysine 6 residue of human CHMP2B, a key ESCRT-III component, at the ICB, impacting the dynamic relocation of CHMP2B to sites of abscission. SMYD2 loss-of-function (genetically or pharmacologically) causes CHMP2B hypomethylation, delayed CHMP2B polymerization and delayed abscission. This is phenocopied by CHMP2B lysine 6 mutants that cannot be methylated. Conversely, SMYD2 gain-of-function causes CHMP2B hypermethylation and accelerated abscission, specifically in cells undergoing cytokinetic challenges, thereby bypassing the abscission checkpoint. Additional experiments highlight the importance of CHMP2B methylation beyond cytokinesis, namely during ESCRT-III-mediated HIV-1 budding. We propose that lysine methylation signaling fine-tunes the ESCRT-III machinery to regulate the timing of cytokinetic abscission and other ESCRT-III dependent functions.

Date: 2024
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DOI: 10.1038/s41467-024-47717-3

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