Mutant embryos have axons ectopically crossing the midline in the central nervous system.
Embryos which are derived from homozygous female germline clones but are paternally rescued have relatively normal central nervous system development, with occasional collapsed longitudinal axons and gaps in axon bundles. Embryos lacking both maternal and zygotic Abl function have severe disruptions in central nervous system development. Most show loss of commissural axons and some have defects in both longitudinal and commissural axons. Embryos lacking both maternal and zygotic Abl function show striking defects in the cellular events of dorsal closure. Leading edge cells do not elongate uniformly and some cells have overly broad or narrowed leading edges. Cells lateral to the leading edge elongate (as occurs in wild type), but do so nonuniformly. Some cells completely fail to change shape. The epithelial sheets often fail to align properly at the midline once dorsal closure is complete. Some mutants initiate dorsal closure even though they have not completed germband retraction. Some cells in the embryos become multinucleate due to defects in cellularisation. Actin enrichment is not uniform at the leading edge during dorsal closure. Dorsal closure is substantially slowed in embryos lacking both maternal and zygotic Abl function, taking two to three times longer than normal. The dorsal/ventral extent of the amnioserosa is larger in the mutant embryos compared to wild type. As closure proceeds, the leading edge of the lateral epidermis folds under the more lateral cells that follow it, suggesting that the leading edge cells do not migrate towards one another at an appropriate rate. Filopodial extensions from epidermal and amnioserosa cells are present in the mutant embryos.