Homozygous stage 16 embryos show a strong defect in myoblast fusion.
sizC1-28/sizU112 embryos show a strong defect in myoblast fusion.
The number of commissural fibers crossing the ventral midline of stage 16 embryos is reduced in sizU112 homozygotes and sizU112/sizC1-28 animals. This effect is seen most strongly in abdominal segments A1-A4. The longitudinal connectives are also thinner. In neuromeres with reduced commissures the midline glial cells migrate toward the connectives. The commissural phenotypes of these embryos are stronger than those of sizC1-28 homozygotes. In stage 16 sizU112/sizC1-28 embryos many axons that usually cross the ventral midline fail to do so and show fasciculation defects.
Mutants show a variable reduction in the number of commissural fibers. Midline glial cell is initially normal but reduced later due to loss of commissural axons.
3-5 neuromeres lack one or both commissures in homozygous embryos.