ArticleNature communications2024
Methylation of ESCRT-III components regulates the timing of cytokinetic abscission.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Large eukaryotic DNA viruses encode ESCRT machinery for membrane remodelling.Nature microbiology · 2026Article
- ESCRT-III function in membrane fission and repair.Nature reviews. Molecular cell biology · 2026Review
- Loss of CHMP2A implicates an ordered assembly of ESCRT-III proteins during cytokinetic abscission.Molecular biology of the cell · 2025Article
- Regulating the balance between GSDMD-mediated pyroptosis and CHMP4B-dependent cell repair attenuates calcium oxalate kidney stone formation.International journal of biological sciences · 2025Article
Corrections and comments
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Authors and funding
16 authors.
Funding
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.
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Registered trials
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