The SCAR and WASp nucleation-promoting factors act sequentially to mediate Drosophila myoblast fusion.

Abstract	The actin nucleation-promoting factors SCAR/WAVE and WASp, together with associated elements, mediate the formation of muscle fibres through myoblast fusion during Drosophila embryogenesis. Our phenotypic analysis, following the disruption of these two pathways, suggests that they function in a sequential manner. Suppressor of cyclic AMP receptor (SCAR) activity is required before the formation of pores in the membranes of fusing cells, whereas Wiskott-Aldrich syndrome protein (WASp) promotes the expansion of nascent pores and completion of the fusion process. Genetic epistasis experiments are consistent with this step-wise temporal progression. Our observations further imply a separate, Rac-dependent role for the SCAR complex in promoting myoblast migration. In keeping with the sequential utilization of the two systems, we observe abnormal accumulations of filamentous actin at the fusion sites when both pathways are disrupted, resembling those present when only SCAR-complex function is impaired. This observation further suggests that actin-filament accumulation at the fusion sites might not depend on Arp2/3 activity altogether.
Authors	Boaz Gildor, R'ada Massarwa, Ben-Zion Shilo, Eyal D Schejter
Journal	EMBO reports (EMBO Rep) Vol. 10 Issue 9 Pg. 1043-50 (Sep 2009) ISSN: 1469-3178 [Electronic] England
PMID	19644501 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Actins Drosophila Proteins Microfilament Proteins SCAR protein, Drosophila WASp protein, Drosophila Wiskott-Aldrich Syndrome Protein
Topics	Actins (metabolism) Animals Cell Fusion Cell Movement Cell Nucleus (metabolism) Drosophila Proteins (genetics, metabolism) Drosophila melanogaster (cytology, embryology, genetics, metabolism) Gene Expression Regulation, Developmental Microfilament Proteins (genetics, metabolism) Microscopy, Electron Myoblasts (cytology, metabolism) Phenotype Wiskott-Aldrich Syndrome Protein (genetics, metabolism)

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