ArticleProceedings of the National Academy of Sciences of the United States of America2020
Actin reduction by MsrB2 is a key component of the cytokinetic abscission checkpoint and prevents tetraploidy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 56 citations in OpenAlex.
- ESCRT-III assembles around mis-segregated DNA to protect genome stability.Nature structural & molecular biology · 2026Article
- Maintaining Genome Integrity: Actin Polymerization Stabilizes Chromatin Bridges in Cytokinesis.International journal of molecular sciences · 2026Review
- Roles of Srs2/PARI-family DNA helicases in NoCut checkpoint signaling and abscission regulation.The Journal of cell biology · 2025Article
- Tension-sensitive LINC-RhoA signaling prevents chromatin bridge breakage in cytokinesis.The EMBO journal · 2025Article
- F-actin disassembly by the oxidoreductase MICAL1 promotes mechano-dependent VWF-GPIbα interaction in platelets.Nature communications · 2025Article
- The role of MICAL2 in cancer progression: mechanisms, challenges, and therapeutic potential.Human cell · 2025Review
- Review
- HIV-1 budding requires cortical actin disassembly by the oxidoreductase MICAL1.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Review
- Cytokinetic abscission requires actin-dependent microtubule severing.Nature communications · 2024Article
- FOXO transcription factors as mediators of stress adaptation.Nature reviews. Molecular cell biology · 2024Review
- The abscission checkpoint senses chromatin bridges through Top2α recruitment to DNA knots.The Journal of cell biology · 2023Article
- Genetic alterations and molecular mechanisms underlying hereditary intrahepatic cholestasis.Frontiers in pharmacology · 2023Review
- MICAL-mediated oxidation of actin and its effects on cytoskeletal and cellular dynamics.Frontiers in cell and developmental biology · 2023Review
- Review
- MICAL1 facilitates pancreatic cancer proliferation, migration, and invasion by activating WNT/β-catenin pathway.Journal of translational medicine · 2022Article
- 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
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abscission is the terminal step of cytokinesis leading to the physical separation of the daughter cells. In response to the abnormal presence of lagging chromatin between dividing cells, an evolutionarily conserved abscission/NoCut checkpoint delays abscission and prevents formation of binucleated cells by stabilizing the cytokinetic intercellular bridge (ICB). How this bridge is stably maintained for hours while the checkpoint is activated is poorly understood and has been proposed to rely on F-actin in the bridge region. Here, we show that actin polymerization is indeed essential for stabilizing the ICB when lagging chromatin is present, but not in normal dividing cells. Mechanistically, we found that a cytosolic pool of human methionine sulfoxide reductase B2 (MsrB2) is strongly recruited at the midbody in response to the presence of lagging chromatin and functions within the ICB to promote actin polymerization there. Consistently, in MsrB2-depleted cells, F-actin levels are decreased in ICBs, and dividing cells with lagging chromatin become binucleated as a consequence of unstable bridges. We further demonstrate that MsrB2 selectively reduces oxidized actin monomers and thereby counteracts MICAL1, an enzyme known to depolymerize actin filaments by direct oxidation. Finally, MsrB2 colocalizes and genetically interacts with the checkpoint components Aurora B and ANCHR, and the abscission delay upon checkpoint activation by nuclear pore defects also depends on MsrB2. Altogether, this work reveals that actin reduction by MsrB2 is a key component of the abscission checkpoint that favors F-actin polymerization and limits tetraploidy, a starting point for tumorigenesis.
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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.