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First published online April 3, 2008
doi: 10.1242/10.1242/jcs.022269

Journal of Cell Science 121, 1303-1313 (2008)
Published by The Company of Biologists 2008
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Research Article

WASP and SCAR have distinct roles in activating the Arp2/3 complex during myoblast fusion

Susanne Berger1,*, Gritt Schäfer1,*, Dörthe A. Kesper1,{ddagger}, Anne Holz2, Therese Eriksson3, Ruth H. Palmer3, Lothar Beck4, Christian Klämbt5, Renate Renkawitz-Pohl1 and Susanne-Filiz Önel1,§

1 Fachbereich Biologie, Entwicklungsbiologie, Philipps-Universität Marburg, Karl-von-Frisch Str. 8, D-35043 Marburg, Germany
2 Institut für Allgemeine und Spezielle Zoologie, Stephanstr. 24, Justus-Liebig-Universität Giessen, D-35390 Giessen, Germany
3 UCMP, Umeå University, Building 6L, 90187 Umeå, Sweden
4 Fachbereich Biologie, Spezielle Zoologie, Philipps-Universität Marburg, Karl-von-Frisch Str. 8, D-35043 Marburg, Germany
5 Institut für Neurobiologie, Westfälische Wilhelms-Universität Münster, Badestr. 9, D-48149 Münster, Germany

§ Author for correspondence (e-mail: oenel{at}staff.uni-marburg.de)

Accepted 21 January 2008

Myoblast fusion takes place in two steps in mammals and in Drosophila. First, founder cells (FCs) and fusion-competent myoblasts (FCMs) fuse to form a trinucleated precursor, which then recruits further FCMs. This process depends on the formation of the fusion-restricted myogenic-adhesive structure (FuRMAS), which contains filamentous actin (F-actin) plugs at the sites of cell contact. Fusion relies on the HEM2 (NAP1) homolog Kette, as well as Blow and WASP, a member of the Wiskott-Aldrich-syndrome protein family. Here, we show the identification and characterization of schwächling – a new Arp3-null allele. Ultrastructural analyses demonstrate that Arp3schwächling mutants can form a fusion pore, but fail to integrate the fusing FCM. Double-mutant experiments revealed that fusion is blocked completely in Arp3 and wasp double mutants, suggesting the involvement of a further F-actin regulator. Indeed, double-mutant analyses with scar/WAVE and with the WASP-interacting partner vrp1 (sltr, wip)/WIP show that the F-actin regulator scar also controls F-actin formation during myoblast fusion. Furthermore, the synergistic phenotype observed in Arp3 wasp and in scar vrp1 double mutants suggests that WASP and SCAR have distinct roles in controlling F-actin formation. From these findings we derived a new model for actin regulation during myoblast fusion.

Key words: Drosophila, Myogenesis, F-actin, Arp3, FuRMAS, Actin cytoskeleton, kette


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