Expression of sliScer\UAS.cKa in the visceral mesoderm during salivary gland migration, driven by Scer\GAL4bap.3, causes glands to curve ventrally, away from the visceral mesoderm.
Expression of sliScer\UAS.cKa under the control of Scer\GAL4C321c results in stalls and premature turns in 37% of the ganglionic branches. The longitudinal tracts in these embryos appear to form normally. Expression of sliScer\UAS.cKa under the control of Scer\GAL4en-e16E results in defects in 23% of the dorsal trunk tracheal branches. Expression of sliScer\UAS.cKa under the control of Scer\GAL4twi.PG results in visceral tracheal branches being generated from the T3 tracheal metamere in 11% of embryos (T3 does not normally produce visceral branches).
When expression is driven by Scer\GAL4elav.PLu, old embryos show defasciculation defects and subtle misroutings of longitudinal connectives across the midline. In earlier embryogenesis glial migration is delayed, defective migration along axons and increased glial cell numbers and increased distance from the midline between the connectives. More glia cluster at the site of exit of the axons from the CNS and some interface glia are missing from the connectives. Older embryos have recovered from these defects and look more normal.
sli2 embryos in which the midline has been rescued by expressing sliScer\UAS.cKa under the control of Scer\GAL4sim.P3.7 often show misinsertion of dorsal muscles 1,2, 9 and 10. However, the overall position of these muscles is not dramatically affected in these embryos. Muscles 21 to 23 are largely unaffected although occasionally an extra muscle is seen. 1% of segments show crossing of the midline by muscles 6/7, 54% show abnormal insertion of muscle 5 and 36% show abnormal insertion of muscles 6/7 (either failing to reach their specific muscle insertion sites in the epidermis - 12%, or reaching the epidermis but making abnormal connections - 24%). In sli2 embryos expressing sliScer\UAS.cKa under the control of Scer\GAL4en-e16E, 49% of segments show muscle cells aligned with sites of ectopic sli expression. In sli2 embryos expressing sliScer\UAS.cKa under the control of Scer\GAL4ptc-559.1, 20% of segments show muscle cells aligned with sites of ectopic sli expression.
The initial migration defect seen in the ventral muscle precursors of sli2 embryos is rescued by expression of sliScer\UAS.cKa under the control of Scer\GAL4sim.P3.7. However, striking defects are seen during the second phase, as muscles extend towards their (muscle attachment sites) MASs. Many muscles that normally attach at sli-positive MASs are instead attached to the wrong places in the epidermis. Muscles 6 and 7 either do not reach their MASs or make abnormal connections with the epidermis. Muscle 5 is often missing or is not properly attached at one or both ends. Muscle 4 is also often not properly attached. Expression of sliScer\UAS.cKa under the control of Scer\GAL4en-e16E results in little change in the muscle pattern. Expression of sliScer\UAS.cKa under the control of Scer\GAL4en-e16E in a sli2 background results in dramatic muscle patterning defects. Dorsal muscles 1, 2, 9 and 10 often fail to stretch across each segment and instead align themselves along the stripe of ectopic sli expression.
The central nervous system commissures are thicker and more fuzzy in embryos expressing sliScer\UAS.cKa under the control of Scer\GAL4elav.PLu or Scer\GAL4sca-537.4 than in wild-type embryos. The longitudinal tracts are thiner than normal, the innermost pCC axons aberrantly cross the midline, and in addition, the lateral and medial pathways are affected, also sometimes crossing the midline. When sliScer\UAS.cKa is expressed in the muscles using Scer\GAL4how-24B, most of the ISNb motor axons stall in the vicinity of their target muscles (6, 7, 12 and 13) and fail to innervate them. The morphology of the muscles is normal.