Over-expression of MAN1Scer\UAS.cWa in the wing under the control of Scer\GAL4Bx-MS1096 generates defects in the formation of the ACV and the PCV in 90-95% of the emerging adults. The phenotypes range from 'gaps', where the PCV shows a gap either from L4 or L5, 'points', where the PCV is reduced to a point, or 'PCV absent', and 'CV absent', where the PCV or both CVs are missing. In addition, the tip of the longitudinal vein L4 is often compromised leading to truncations.
Scer\GAL4elav-C155/MAN1UAS.cWa partially rescues MAN1ΔC
Scer\GAL4Mef2.PR/MAN1UAS.cWa partially rescues MAN1ΔC
MAN1UAS.cWa partially rescues MAN1ΔC
The climbing defect of MAN1ΔC flies can be rescued by expression of MAN1Scer\UAS.cWa under the ubiquitous Scer\GAL4Act5C.PI driver.
Expression of MAN1Scer\UAS.cWa within the presynaptic motoneuron, using the neuronal driver Scer\GAL4elav-C155 or within the post-synaptic muscle with the Scer\GAL4Mef2.PR driver is not sufficient to fully restore motor ability.
Partial rescue of MAN1ΔC mutants is observed through the introduction of one or two copies of MAN1Scer\UAS.cWa without a Scer\GAL4 driver. Both motor ability and synaptic phenotypes are partially rescued.
Both the pre- and post-synaptic expression of MAN1Scer\UAS.cWa (under the control of Scer\GAL4Mef2.PR or Scer\GAL4elav-C155 can partially rescue the drop in EPSC amplitude detected in MAN1ΔC larvae.