Mutant stage 16 embryos show a severe myoblast fusion defect in the dorsal pharyngeal muscle.
mbcC1/mbcD11.2 transheterozygote embryos display defects in the migration of the visceral longitudinal muscle founder cells and their morphology as well as the muscle fusion. Late in the embryonic development, the first midgut constriction is missing in the mbcC1/mbcD11.2 mutants.
In homozygous mutant embryos, myoblasts are competent to migrate to the founder cells, but fusion does not occur.
Homozygous embryos exhibit breaks in the outer longitudinal fascicles and a collapse of axons onto the MP1 fascicle tracts. Thinning of the longitudinal axon tracts and abnormal spacing between segments is also observed.
Unfused myoblasts are apparent in stage 16 homozygous embryos. Although the majority of founder cells examined remain mononucleate, a limited amount of fusion does occur, as binucleate muscle precursors that have undergone a single fusion event between a founder cell and a fusion competent myoblast (FCM) are seen in the mutant embryos. The muscle founders analysed and the percentage of segments in which the founder cell remains mononucleate are as follows: DA1 (72.1%), DO1 (76.3%), LO1 (90.2%), LT2 (93.4%), LT4 (95.0%), VT1 (78.9%), VA2 (84.6%). The overall level of myoblast fusion in embryos lacking both maternal and zygotic function is roughly comparable to that seen in zygotic mutant embryos.
The F-actin foci which are seen in wild-type FCMs at points of contact with developing myofibers are less dense and somewhat dispersed in homozygous FCMs. In addition, the actin cytoskeletal network of the mutant FCMs is different from wild type, with many of the mutant cells showing a complete collapse of the network.
The eve-expressing DA1 founder cell undergoes no fusion in mbcD11.2 embryos.
Myoblast fusion is absent in mbcD11.2 zygotic mutant embryos and in embryos derived from mbcD11.2 germline clones.
The extent of myoblast fusion in mbcD11.2 mutant embryos is significantly reduced compared to wild type.
Homozygous embryos do not show any apparent defects in macrophage migration.
When mutant somatic clones are made in border cells, a strong effect is seen on border cell migration. At stage 10 only about 10% of mutant border cell clusters reach the oocyte.