Expression of enScer\UAS.cYa in midline cells, driven by Scer\GAL4sim.PS, prevents the formation of the anterior commissure and interferes with the differentiation of midline glia.
Nearly half of midline precursors that express enScer\UAS.cYa under the control of Scer\GAL4sim.PS either generate only two undifferentiated cells or generate progeny that die during embryogenesis. Any surviving progeny are abnormally positioned at the dorsal surface of the CNS. Scer\GAL4sim.PS>enScer\UAS.cYa-expressing midline cells rarely develop into midline glia and the glial cells fail to enwrap the remaining, posterior, commissure. MP1 interneurons are never observable in these embryos. UMI neurons show slight axonal pathfinding defects. Axon guidance of VUM motoneurons is severely affected; in wild-type embryos these axons bifurcate at the anterior commissure but in Scer\GAL4sim.PS>enScer\UAS.cYa embryos, these axons turn randomly to one side of the CNS and bifurcate in the wrong location. Most of the VUM interneurons also project to only one side.
Hindgut boundary cell rows and the anterior boundary cell ring are missing in embryos expressing enScer\UAS.cYa under the control of Scer\GAL4byn-Gal4. The posterior boundary cell ring is still present in these embryos.
84% of flies expressing enScer\UAS.cYa under the control of Scer\GAL4ey.PH are wild type. Some animals are seen in which most of the head and one or both eyes of reduced size are present.
The incipient anterior commissure (AC) and posterior commissure (PC) show little separation in stage 13 embryos expressing enScer\UAS.cYa under the control of Scer\GAL4elav-C155, in contrast to wild-type embryos which show separation of the incipient AC and PC at the lateral extremes of the single midline commissure at this stage. The central nervous system (CNS) is narrower from side to side but thicker in the dorsoventral dimension in stage 16 embryos expressing enScer\UAS.cYa under the control of Scer\GAL4elav-C155 compared to control embryos. The segmental and intersegmental nerves are missing or reduced in over half the neuromeres and exit the CNS at aberrant locations. The intersegmental connectives are thinner than normal, and the AC and PC are completely or partially fused. RP motor neurons show a range of defects. Fas2-positive longitudinal fascicles are severely disrupted. The MP1 pathway is thinner than normal, the lateral fascicle is present in only some hemisegments and the FN3 fascicle is missing. The development of neuromuscular junctions is abnormal. Motor neuron growth cones occur in only a fraction of hemisegments, in contrast to wild-type. The growth cones show a graduation of shapes. Most have sparse filopodial contact with the muscles or are collapsed or club-like in shape. The growth cones extend over an area one-third to one-half the area seen in control embryos. A full complement of sensory neurons is present in embryos expressing enScer\UAS.cYa under the control of Scer\GAL4elav-C155, but the nerves and central fascicles containing their processes are disorganised. Peripheral nerves are "frayed" or the connections between afferent and efferent fibres are completely missing. Axons of the SNa and SNc motor neurons contact muscle fibres near their normal locations in embryos expressing enScer\UAS.cYa under the control of Scer\GAL4how-24B.