Homozygous embryos show a myoblast fusion defect. The average number of eve-positive nuclei per DA1 muscle is only 5.6 +/- 1.2, compared to the wild-type number of 10.7 +/- 1.6. Muscle cell fate specification, fusion competent myoblast (FCMs) migration and muscle cell adhesion appear normal in the mutant embryos.

The myoblast fusion defect seen in homozygous embryos is only slightly exacerbated if the embryos are derived from homozygous female germline clones (and thus lack maternal function in addition to lacking zygotic function).

A large number of F-actin foci per hemisegment remain in late stage 14 zygotically mutant embryos, in contrast to wild type, where the number of foci have significantly decreased by stage 15. The F-actin foci are generated in the FCMs (as in wild type), but have a more dispersed morphology than normal. The F-actin rich area in the mutant FCM extends further back into the cytoplasm compared to wild type (where it is restricted to the protrusive tip) and is decorated with an increased number of ribosomes, indicating the presence of loosely packed actin filaments. Most of the F-actin foci in late stage 14 mutant embryos are not associated with any inward curvature of the apposing founder cell/myotube membrane, suggesting that they fail to invade these cells (as occurs in wild type). A GFP diffusion assay and EM analysis suggest that fusion pore formation is blocked in the mutant embryos.

Expression of Pak3^{K322A.Scer\UAS.C.T:SV5\V5} under the control of Scer\GAL4^twi.PG in a Pak3^del background results in an almost complete failure of myoblast fusion in embryos.

Pak3^del has embryonic myoblast phenotype, suppressible | partially by Scer\GAL4^twi.PG/Pak^UAS.Tag:V5

Pak3^del is an enhancer of embryonic myoblast phenotype of SCAR^Δ37