ArticleCell reports2023
Anillin forms linear structures and facilitates furrow ingression after septin and formin depletion.
Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- F-actin organization excludes E-cadherin from the division furrow to ensure cytokinesis fidelity.Life science alliance · 2026Article
- A cortical pool of LIN-5 (NuMA) controls cytokinetic furrow formation and cytokinesis completion.The Journal of cell biology · 2025Article
- Anillin mediates unilateral furrowing during cytokinesis by limiting RhoA binding to its effectors.The Journal of cell biology · 2025Article
- Germ fate determinants protect germ precursor cell division by reducing septin and anillin levels at the cell division plane.Molecular biology of the cell · 2024Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
During cytokinesis, a contractile ring consisting of unbranched filamentous actin (F-actin) and myosin II constricts at the cell equator. Unbranched F-actin is generated by formin, and without formin no cleavage furrow forms. In Caenorhabditis elegans, depletion of septin restores furrow ingression in formin mutants. How the cleavage furrow ingresses without a detectable unbranched F-actin ring is unknown. We report that, in this setting, anillin (ANI-1) forms a meshwork of circumferentially aligned linear structures decorated by non-muscle myosin II (NMY-2). Analysis of ANI-1 deletion mutants reveals that its disordered N-terminal half is required for linear structure formation and sufficient for furrow ingression. NMY-2 promotes the circumferential alignment of the linear ANI-1 structures and interacts with various lipids, suggesting that NMY-2 links the ANI-1 network with the plasma membrane. Collectively, our data reveal a compensatory mechanism, mediated by ANI-1 linear structures and membrane-bound NMY-2, that promotes furrowing when unbranched F-actin polymerization is compromised.
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Registered trials
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