85% of hemisegments show detachment of ISN motor axons from sensory nerves of the anterior fascicle in embryos expressing sideScer\UAS.cSa under the control of Scer\GAL4Mef2.PR. The growth cone of the ISN splits aberrantly into several directions in embryos expressing sideScer\UAS.cSa under the control of Scer\GAL4Mef2.PR. The split growth cones prevent dorsal migration, resulting in strongly reduced growth rates.
Most, if not all, ISN growth cones are tightly attached to tracheal branches in sideC137/sideI1563 embryos expressing sideScer\UAS.cSa in the trachea under the control of Scer\GAL4btl.PS. The ISN follows the tracheal substrate in these embryos and crosses and re-crosses the transverse connective.
Most, if not all, ISN growth cones are attached to hemocytes in sideC137/sideI1563 embryos expressing sideScer\UAS.cSa in the hemocytes under the control of Scer\GAL4srp (this does not occur in wild-type embryos). Filopodial extensions of both cell membranes are tightly interdigitated.
Third instar larvae expressing sideScer\UAS.cSa under the control of Scer\GAL4how-24B often lack neuromuscular junctions (NMJs) on dorsal muscles (the percentage of muscles lacking NMJs is given in parentheses); muscle 1 (88%), muscle 9 (88%), muscle 2 (39%), muscle 10 (39%).
Third instar larvae expressing sideScer\UAS.cSa under the control of Scer\GAL4Mef2.PR often lack neuromuscular junctions (NMJs) on dorsal muscles (the percentage of muscles lacking NMJs is given in parentheses); muscle 1 (93%), muscle 9 (93%), muscle 2 (60%), muscle 10 (57%).
Expression of sideScer\UAS.cSa under the control of Scer\GAL4elav.PLu in sideD609 embryos exacerbates the sideD609 mutant phenotype, particularly in those branches of the motor projection that are less disrupted in sideD609 embryos; failure to innervate the lateral musculature is increased for both the dorsal and lateral SNa branches and the ISN stalls earlier and more frequently. The ISNb, ISNd and SNc branches are largely absent. These gain of function phenotypes are more severe than those seen when sideScer\UAS.cSa is expressed under the control of Scer\GAL4elav.PLu in a wild-type background. Expression of sideScer\UAS.cSa under the control of Scer\GAL4elav.PLu in a wild-type background can phenocopy the side loss of function phenotype. The ISN is still at the first branch choice point at the stage where it would be at the final choice point in wild-type embryos. Innervation is also still lacking for much of the ventral musculature well into stage 16, with the ISNb and ISNd absent in each segment and ISNc greatly reduced. The formation of the Fas2-positive longitudinal fascicles remains normal. Expression of sideScer\UAS.cSa in the trachea under the control of Scer\GAL4C38 results in an ISN phenotype; the ISN continues tracking the trachea beyond muscle 4 out to the dorsal musculature. Abnormal exploration of the main tracheal trunk by these motor axons is seen in the region of the dorsal musculature. The development of the ISNb can be perturbed by contact with side-expressing trachea and tracheoles. Expression of sideScer\UAS.cSa under the control of Scer\GAL4C142 does not alter motor axon targeting. Expression of sideScer\UAS.cSa under the control of Scer\GAL4l(3)H94-H94 results in ISNb axons being strongly attracted to muscle 13. By the end of embryogenesis, innervation is present for all muscles in the ventral muscle domain, although innervation is still higher on muscle 13.
Scer\GAL4Mef2.PR, sideUAS.cSa has muscle cell of A1-7 dorsal acute muscle 1 phenotype, suppressible by beat-IaUAS.cFa/Scer\GAL4Mef2.PR
Scer\GAL4Mef2.PR, sideUAS.cSa has muscle cell of A1-7 dorsal acute muscle 2 phenotype, suppressible by beat-IaUAS.cFa/Scer\GAL4Mef2.PR
Scer\GAL4Mef2.PR, sideUAS.cSa has muscle cell of A1-7 dorsal oblique muscle 1 phenotype, suppressible by beat-IaUAS.cFa/Scer\GAL4Mef2.PR
Scer\GAL4Mef2.PR, sideUAS.cSa has muscle cell of A1-7 dorsal oblique muscle 2 phenotype, suppressible by beat-IaUAS.cFa/Scer\GAL4Mef2.PR
Co-expression of beat-IaScer\UAS.cFa suppresses the lack of neuromuscular junctions seen on dorsal muscles which is caused by expression of sideScer\UAS.cSa under the control of Scer\GAL4Mef2.PR.
The neuromuscular junction innervation defects seen in the dorsal muscles of beat-Ia3/beat-IaC163 third instar larvae are not enhanced by expression of sideScer\UAS.cSa under the control of either Scer\GAL4how-24B or Scer\GAL4Mef2.PR.
Scer\GAL4C142/sideUAS.cSa partially rescues sideD609
sideUAS.cSa/Scer\GAL4elav.PLu fails to rescue sideD609
Expression of sideScer\UAS.cSa under the control of Scer\GAL4C142 in sideD609 embryos results in reversion of most branches of the motor projection towards wild type.
