Expressing Nlg1^UAS.cBa under the control of Scer\GAL4^Mef2.PR leads to axonal growth defects in persistent motor neurons which innervate the abdominal lateral tergosternal muscles at pupal and pharate adult stages. At 33-35 hours after puparium formation axon terminals appear compacted, with distal branches transformed into flattened growth cones with many filopodia. In late pharate adults, axons display reduced branch length, territory and complexity, and maintain greater than usual numbers of filopodia. In adults there is a slight (but significant) increase in presynaptic active zones compared to wild-type controls.

At 35 hours after puparium formation and in late pharate adults, axonal branches growing on somatic muscle clones expressing Nlg1^UAS.cBa under the control of Scer\GAL4^Mef2.PR display the same hyper-stabilisation phenotype seen in fully expressing flies, while branches from the same neuron growing on non-clonal muscle appear wild-type.

Expressing Nlg1^UAS.cBa under the control of Scer\GAL4^Mef2.PR disrupts the physiology of abdominal lateral tergosternal muscles in late pharate adults. Calcium events are asynchronous across the muscle field and are restricted to small muscle subsets.

Expressing Nlg1^UAS.cBa under the control of Scer\GAL4^ppk.PG results in the misrouting of axons from persistent motor neurons which normally innervate the abdominal lateral tergosternal muscles in pharate adults. Motor neuron axons grow between muscle fibres (perpendicular to the plane of wild-type arborisations), contact the dendrites of vdaa multidendritic sensory neurons and establish ectopic brp-positive presynaptic active zones.

The neuromuscular junctions of larvae expressing Nlg1^Scer\UAS.cBa under the control of Scer\GAL4^Mef2.PR are smaller than normal. The average bouton number per muscle area is significantly reduced compared to controls.