ArticleeLife2021
Identification of abscission checkpoint bodies as structures that regulate ESCRT factors to control abscission timing.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 28 citations in OpenAlex.
- ESCRT-III function in membrane fission and repair.Nature reviews. Molecular cell biology · 2026Review
- MOS is a key regulator of meiotic midbody assembly and prevents abnormal divisions in mouse eggs and their polar bodies.Journal of cell science · 2026Article
- Roles of Srs2/PARI-family DNA helicases in NoCut checkpoint signaling and abscission regulation.The Journal of cell biology · 2025Article
- RNA splicing is required for timely completion of abscission and is modulated by the abscission checkpoint.bioRxiv : the preprint server for biology · 2025Article
- Review
- Methylation of ESCRT-III components regulates the timing of cytokinetic abscission.Nature communications · 2024Article
- Cytokinetic abscission requires actin-dependent microtubule severing.Nature communications · 2024Article
- Article
- Reversible phase separation of ESCRT protein ALIX through tyrosine phosphorylation.Science advances · 2023Article
- Chaperone-Dependent Degradation of Cdc42 Promotes Cell Polarity and Shields the Protein from Aggregation.Molecular and cellular biology · 2023Article
- Article
- Caveolae promote successful abscission by controlling intercellular bridge tension during cytokinesis.Science advances · 2022Article
- Mechanics and regulation of cytokinetic abscission.Frontiers in cell and developmental biology · 2022Review
- Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The abscission checkpoint regulates the ESCRT membrane fission machinery and thereby delays cytokinetic abscission to protect genomic integrity in response to residual mitotic errors. The checkpoint is maintained by Aurora B kinase, which phosphorylates multiple targets, including CHMP4C, a regulatory ESCRT-III subunit necessary for this checkpoint. We now report the discovery that cytoplasmic abscission checkpoint bodies (ACBs) containing phospho-Aurora B and tri-phospho-CHMP4C develop during an active checkpoint. ACBs are derived from mitotic interchromatin granules, transient mitotic structures whose components are housed in splicing-related nuclear speckles during interphase. ACB formation requires CHMP4C, and the ESCRT factor ALIX also contributes. ACB formation is conserved across cell types and under multiple circumstances that activate the checkpoint. Finally, ACBs retain a population of ALIX, and their presence correlates with delayed abscission and delayed recruitment of ALIX to the midbody where it would normally promote abscission. Thus, a cytoplasmic mechanism helps regulate midbody machinery to delay abscission.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.