Mutant larvae show an increased penetration of 3kD fluorescein-dextran into the ventral nerve cord in a permeability assay compared to the dye penetration seen in control larvae.
10 kDa labeled dextran molecules can easily penetrate into the CNS in Df(1)moody-Δ17 mutant embryos.
Stage 17 homozygous embryos show loss of the blood brain barrier (assayed by studying dextran uptake in living embryos).
Only ~1% of homozygous females and hemizygous males survive to adulthood. These survivors show severe motor defects and have a reduced lifespan compared to wild-type flies. These flies show a breakdown of the blood-brain barrier, as assessed by the penetrance of a fluorescent dye into the retina.
Df(1)moody-Δ17 mutants are able to hatch but show mildly uncoordinated motor behaviour and die during larval or pupal stages. The formation of the blood-brain barrier is defective, as shown by penetration of fluorescent dye into the nerve cord. Although the normal complement of surface glia is found at the surface of the nerve cord in Df(1)moody-Δ17 mutants, these glia show a number of defects. They are irregular in size and shape with a disrupted cortical cytoskeleton at the cell cortex and variably-positioned nuclei. Additionally, the septate junctions are significantly shorter in length and less organized than in wild-type glia.
