Homozygous Df(2L)200 mutant embryos display intersegmental nerve b (ISNb) defects.
Df(2L)200 mutants exhibit a striking increase in the size of crystal cell clusters and the presence of numerous ectopic Dox-A3-positive cells scattered throughout the embryo. Most hemocytes do not acquire the crystal cell fate in Df(2L)200 embryos, with only average about 90 crystal cells, compared to approximately 250 in wild-type, with 40% of the 90 cells mislocated. In embryos derived from Df(2L)200 germline clones exhibit ectopic crystal cells, while most hemocytes do not differentiate as crystal cells. In a stg2 mutant context, Df(2L)200 mutant embryos induce a twofold increase in the number of crystal cells.
Glial cell development is affected in Df(2L)200 mosaic larvae and many R2-R5 axons fail to terminate in the lamina and instead project into the medulla.
In Df(2L)200 mosaic mutants, lamina precursor cells fail to divide and undergo cell death at a greater rate than wild type. The neuronal phenotype is cell autonomous.
Homozygous embryos show a 60% reduction in the number of Pxn-positive hemocytes compared to wild type and the hemocytes have abnormal morphologies and migration behaviour; they fail to migrate ventrally past the 2nd thoracic segment and those that migrate dorsally stay clumped together along the dorsal boundary of the epidermis. Most of the hemocytes in stage 16 homozygous embryos remain small and irregular in shape, in contrast to wild-type where they are enlarged due to phagocytic activity.