70% of stage 15 DrΔ68 mutant embryos show defects in brain development. These defects range from a gap between the deutocerebral brain region and the neuromeres of the posterior subesophageal ganglion to a reduction in neuronal tissue in the tritocerebrum.
Severe axonal pattering disruption is seen in DrΔ68 stage 15 embryos. Cervical connectives that run from the deutocerebral and tritocerebral neuromeres to the subesophageal ganglion are reduced or missing and the tritocerebral commissure is disrupted. Defects are also seen in the longitudinal axon tracts in the subesophageal ganglion.
DrΔ68 stage 15 embryos show reduction or loss of basal procephalic glia associated with both cervical and longitudinal tracts. Neuropile glial loss is seen in the tritocerebral, protocerebral and deutocerebral neuromeres. The frontal connective is severely reduced or missing whereas the supraesophageal commissure appears normal. Surface and cortex glia are unaffected.
In DrΔ68 stage 12 embryos there is severe loss of basal procephalic longitudinal glia cells. The deuto-/tritocerebral (D/T) fibre tract founder cluster is decreased in size and tract formation in the tritocerebrum is impaired.
No significant change in the amount of proliferation in the tritocerebrum is seen in DrΔ68 stage 12 embryos compared to wild type.
Mutant stage 12 embryos show a reduction in the number of glial cells in the deutocerebrum and tritocerebrum compared to wild-type embryos, but the number of glial cells in the protocerebrum is unchanged.
DrΔ68 mitotic recombination clones induced at 0-24hrs after egg laying are generally lethal. Clones induced at 24-48hrs after egg laying are viable. In the wing-disc derivatives, clone-associated defects are displayed in the wing hinge, the posterior scutum and the scutellum. At the hinge, the most frequently observed anomalies are malformations ranging from small defects such as an outheld wing, to the partial loss of proximal hinge structures, or to even the complete loss of most hinge structures, namely sclerites, and the proximal dorsal radius. In the most extreme cases, the wing is fused to the scutellum and scutum, or is displaced posteriorly. Generally, the tegula is not affected. Clone induction between 48-72hrs after egg laying yields similar results. In addition, approximately 19% of flies with visible clones display ectopic tissue carrying macro- and microchaetae, indicating a notum identity. The ectopic notal tissue appears dorsal to the hinge and contiguous to it. At the notum, when DrΔ68 minute+ clones are induced at 24-48hrs after egg laying, the most frequent anomalies are a reduction of the scutellum and the appearance of depigmented, naked, and corrugated cuticle in the lateral posterior scutum adjacent to the allula and the hinge. DrΔ68 mitotic recombination clones frequently develop extra macrochaetae, mostly in the dorsocentral region of the notum and in the scutellum. Occasionally, these clones also induce nearby wild-type cells to differentiate as chaetae. The clones also suppress extant chaetae, the anterior and posterior supraalar bristles being the most affected, and interfere with the correct formation of the scuto-scutellar suture. In clones that comprise the lateral anterior notum, the anterior and posterior notopleural and the presutural macrochaetae are missing in 70, 10 and 15% of cases, respectively. DrΔ68 minute+ clones in the dorsal hinge exhibit a shortening of the distance between the sc-positive proneural cluster at dorsal radius, in the hinge, and the anterior postalar cluster, in the lateral notum. The distal and proximal sc-positive clusters of the tegula region also appear to be fused. The fold of the disc, that separates the notum and hinge regions is absent when these regions are mutant for DrΔ68.
Homozygous clones have no aberrant phenotype in the ventral surface of the wing, but result in the transformation of dorsal wing structures into a ventral fate. The dorsal anterior wing margin differentiates ventral bristles (a single row of thin bristles interspersed with chemosensory bristles at every fifth position is seen). The dorsal surface of the alula differentiates bristles, reflecting a transformation to the ventral fate. Veins L2 and L4 are corrugated on the dorsal surface and differentiate three rows of strongly pigmented cells, mimicking the ventral pattern. Veins L3 and L5 differentiate ventral characteristics on the dorsal surface, losing pigmentation and consisting of a single row of aligned cells on the dorsal surface.
The segmental border muscles are enlarged and almost all Kr-positive lateral muscle precursors (LT2 and LT4) are absent in mutant embryos.
Embryos exhibit defects in the formation of dorsal muscles 9 and 10, lateral muscles 21-24 and ventral external muscles 26, 27 and 29.
Neuroblast NB6-4 forms normally in homozygous embryos, although the timing and pattern of its subsequent divisions to produce the glial cells MM-CBG and M-CBG appear abnormal. Medial migration of MM-CBG and M-CBG is often retarded, or fails to occur, and the morphology of these cells is abnormal. The PM and PQ neurons are often located abnormally and have abnormal morphology.
DrΔ68 is rescued by Scer\GAL4how-24B/DrUAS.cIa
Scer\GAL4how-24B-mediated expression of DrScer\UAS.cIa rescues the lateral muscle phenotype.
