bk1 << l(3)93Dm << E(Egfr)C22 << bk2 << sar1
Homozygous embryos show defects in commissure formation. The commissures are tightly fasciculated into a single bundle in late stage 12 and early stage 13 embryos and remain poorly separated into mid-stage 13 (in contrast to wild-type embryos which show clear commissural separation by mid-stage 13). Partial commissural fusions and distortions remain common in late stage 13 and early stage 14 homozygous embryos. The commissural axons form a dense bundle at the dorsal boundary of the nerve cord in homozygotes (in contrast to wild type where they interdigitate amongst the midline glia). The commissural bundles are thicker and the longitudinal fibres are sparser than normal. The pCC axon does not extend as far anteriorly in homozygous embryos as in wild type at stage 12/1, and appears stalled after minimal outgrowth. The pCC axon frequently remains stalled at early stage 13, although many late stage 13 embryos show nearly normal extension of the pCC axon into the next anterior segment. 95% of embryos show delayed longitudinal growth in, on average, more than 50% of their segments. Additional morphological defects are seen by mid to late stage 14 in homozygous embryos. The formation of midgut constrictions is blocked, resulting in a large, poorly organised gut. The midgut mass displaces and fragments the nerve cord, particularly in upper abdominal segments, resulting in both commissural and longitudinal discontinuities in the nerve cord.
Homozygous embryos die before hatching.