ArticleScientific reports2017
Non-muscle myosin II is required for correct fate specification in the Caenorhabditis elegans seam cell divisions.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- myh9b is a critical non-muscle myosin II encoding gene that interacts with myh9a and myh10 during zebrafish development in both compensatory and redundant pathways.G3 (Bethesda, Md.) · 2025Article
- UBR-5 and UBE2D mediate timely exit from stem fate via destabilization of poly(A)-binding protein PABP-2 in cell state transition.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Unconventional Myosins fromBiomolecules · 2022Review
- A transient apical extracellular matrix relays cytoskeletal patterns to shape permanent acellular ridges on the surface of adult C. elegans.PLoS genetics · 2022Article
- Non-muscle Myosin II: Role in Microbial Infection and Its Potential as a Therapeutic Target.Frontiers in microbiology · 2019Review
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Authors and funding
2 authors.
Funding
Abstract
During development, cell division often generates two daughters with different developmental fates. Distinct daughter identities can result from the physical polarity and size asymmetry itself, as well as the subsequent activation of distinct fate programmes in each daughter. Asymmetric divisions are a feature of the C. elegans seam lineage, in which a series of post-embryonic, stem-like asymmetric divisions give rise to an anterior daughter that differentiates and a posterior daughter that continues to divide. Here we have investigated the role of non-muscle myosin II (nmy-2) in these asymmetric divisions. We show that nmy-2 does not appear to be involved in generating physical division asymmetry, but nonetheless is important for specifying differential cell fate. While cell polarity appears normal, and chromosome and furrow positioning remains unchanged when nmy-2 is inactivated, seam cell loss occurs through inappropriate terminal differentiation of posterior daughters. This reveals a role for nmy-2 in cell fate determination not obviously linked to the primary polarity determination mechanisms it has been previously associated with.
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