WASP and SCAR have distinct roles in activating the Arp2/3 complex during myoblast fusion
2008 (English)In: Journal of Cell Science, ISSN 0021-9533, E-ISSN 1477-9137, Vol. 121, no Pt 8, 1303-1313 p.Article in journal (Refereed) Published
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 Arp3 schwächling 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.
Place, publisher, year, edition, pages
2008. Vol. 121, no Pt 8, 1303-1313 p.
Drosophila, Myogenesis, F-actin, Arp3, FuRMAS, Actin cytoskeleton, kette
Cell and Molecular Biology
Research subject Molecular Biology
IdentifiersURN: urn:nbn:se:umu:diva-20623DOI: 10.1242/jcs.022269PubMedID: 18388318OAI: oai:DiVA.org:umu-20623DiVA: diva2:209175