ArticleJournal of cell science2016
Drosophila Kette coordinates myoblast junction dissolution and the ratio of Scar-to-WASp during myoblast fusion.
Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- NCKAP1 coordinates focal adhesion and adherens junction dynamics in endothelial barrier maintenance and angiogenesis.iScience · 2026Article
- ARP2/3 Regulates Fatty Acid Synthesis by Modulating Lipid Droplets' Motility.International journal of molecular sciences · 2022Article
- Review
- Rhes Tunnels: A Radical New Way of Communication in the Brain's Striatum?BioEssays : news and reviews in molecular, cellular and developmental biology · 2020Review
- Review
- Serpent/dGATAb regulates Laminin B1 and Laminin B2 expression during Drosophila embryogenesis.Scientific reports · 2019Article
- RNAi Screen inG3 (Bethesda, Md.) · 2019Article
- β-Catenin is essential for differentiation of primary myoblasts via cooperation with MyoD and α-catenin.Development (Cambridge, England) · 2019Article
- Acting on identity: Myoblast fusion and the formation of the syncytial muscle fiber.Seminars in cell & developmental biology · 2017Review
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The fusion of founder cells and fusion-competent myoblasts (FCMs) is crucial for muscle formation in Drosophila Characteristic events of myoblast fusion include the recognition and adhesion of myoblasts, and the formation of branched F-actin by the Arp2/3 complex at the site of cell-cell contact. At the ultrastructural level, these events are reflected by the appearance of finger-like protrusions and electron-dense plaques that appear prior to fusion. Severe defects in myoblast fusion are caused by the loss of Kette (a homolog of Nap1 and Hem-2, also known as NCKAP1 and NCKAP1L, respectively), a member of the regulatory complex formed by Scar or WAVE proteins (represented by the single protein, Scar, in flies). kette mutants form finger-like protrusions, but the electron-dense plaques are extended. Here, we show that the electron-dense plaques in wild-type and kette mutant myoblasts resemble other electron-dense structures that are known to function as cellular junctions. Furthermore, analysis of double mutants and attempts to rescue the kette mutant phenotype with N-cadherin, wasp and genes of members of the regulatory Scar complex revealed that Kette has two functions during myoblast fusion. First, Kette controls the dissolution of electron-dense plaques. Second, Kette controls the ratio of the Arp2/3 activators Scar and WASp in FCMs.
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Registered trials
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