Scer\GAL4sim.P3.7- or Scer\GAL4pros.C20-mediated expression of DΔHMG.Scer\UAS results in embryos with collapsed commissures, reduced separation between longitudinal tracts, gaps in longitudinal connectives, misrouting and inappropriate midline crossing by longitudinal axons. 50-70% of embryos exhibit some degree of CNS disruption.
The strong embryonic CNS defects of Dr72/Df(3L)fz-GS1a animals are made worse when DΔHMG.Scer\UASis expressed via Scer\GAL4sim.P3.7 in this background.