Mutant embryos show decelerated and irregular outgrowth of the visceral mesoderm. Many unfused myoblasts surround the visceral mesoderm in the mutant embryos.
mbcC1 mutants show enlarged foci, as well as increased numbers of actin foci. Enlarged foci are seen in these mutants from the earliest stages of fusion and foci persist after fusion would be complete in wild-type.
In mbcC1 mutant embryos, the secretory star cells (stellate cells) integrate into the developing Malpighian tubule epithelium but are reduced in number. The tubules themselves exhibit severe misguidance defects. Tha anterior tubules are shortened and knotted.
Homozygous embryos do not show any apparent defects in macrophage migration.
No somatic muscle cell fusion occurs in mbcC1 mutant embryo, leaving only mononucleated myoblasts.
In mutant embryos, syncytia within somatic muscles are almost absent. Mutants show defects in the formation of midgut constrictions, and show severe abnormalities in the formation of visceral muscles. At stage 12 the visceral band is randomly interrupted and the elongated Fas3 expressing cells seem to be disorientated. During further development parts of the visceral band either stretch out in the dorsal ventral direction (as in wild-type) or form disarranged patches. The number of myoblast founder cells appears to be reduced, and large gaps are visible in the visceral band. Many globular cells are seen at the margin of the visceral band that appear to be unfused myoblasts. No myoblast fusion is detectable. While the circular musculature shows severe defects and is apparently reduced, the longitudinal musculature is completely absent at the end of embryogenesis.
Syncytia are not seen in the midgut musculature of mutant embryos. Two classes of fibres are apparent (as in wild type) - elongated, longitudinal cells and smaller circular fibres at right angles to them, but in contrast to wild type these fibres are mononucleate in mutant embryos. Elongated circular muscle founder cells and unfused myoblasts become closely apposed in the visceral mesoderm of developing embryos, but them fail to fuse.
The development of multinucleate muscles is blocked in mutant embryos, but tendon cells are specified normally.
Myoblasts fail to fuse and form loose clusters of cells in locations roughly corresponding to the ventral, lateral and dorsal muscle groups. They are in random orientation relative to pioneer cells. Myoblasts exhibit near complete absence of prefusion complexes, an occasional complex can be seen at apparently random locations. The complex is wild type, showing no defects. Most unfused cells are cleared by macrophages by the end of stage 16.
Embryos homozygous for the mbcC1 chromosome (or heterozygous for mbcC1 and Df(3R)mbc-R1), show a variably expressed 'dorsal open' phenotype.
Fusion of myoblasts to form myotubes is virtually absent (development of syncytial muscles is blocked), but muscle founder cells form and later elongate, make epidermal contacts and develop into mononucleate muscles that express differentiated muscle markers. Limited number of neuromuscular synapses form and their ultrastructure is identical to the wild type, EJCs demonstrate the junctions are functional.
Embryos lie motionless in the vitelline membrane and fail to hatch. Examination with polarised light reveals a lack of differentiated muscle. Myoblasts fail to fuse. At 13 to 14 hours of development the myoblasts lie in a segmental array. At 16 to 17 hours of development the myoblasts fall into two populations, stretched and rounded. Stretched myoblasts first appear at around 11 hours after egg laying, and eventually can span distances two or three times the length of normal muscles. They often occur at positions and in orientations reminiscent of wild type muscle precursors. Only very few fusions occur. Segregation and movement of slou-expressing founder cells and vg-expressing cells is normal.
Epidermal development and differentiation are normal.