The fusion of founder (FCs) and fusion-competent myoblasts (FCMs) is crucial for muscle formation in Drosophila. Characteristic events of myoblast fusion are 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 member of the regulatory Scar/WAVE complex. 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/WAVE 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/WAVE and WASp in FCMs.
- Received June 10, 2015.
- Accepted July 25, 2016.
- © 2016. Published by The Company of Biologists Ltd
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