Expression of Nrg^GPI.Scer\UAS pre-synaptically, under the control of Scer\GAL4^c17 does not rescue the physiological Nrg⁸⁴⁹ mutant phenotype.

Expression of Nrg^GPI.Scer\UAS post-synaptically, under the control of Scer\GAL4^{shakB.lethal.4.1} does not rescue the physiological Nrg⁸⁴⁹ mutant phenotype.

Expression of Nrg^GPI.Scer\UAS pre- and post-synaptically, under the control of Scer\GAL4^A307 does not rescue the physiological Nrg⁸⁴⁹ mutant phenotype.

Overexpression of Nrg^GPI.Scer\UAS in a wild-type background, either pre- or post-synaptically (under the control of Scer\GAL4^c17 or Scer\GAL4^{shakB.lethal.4.1} respectively) has a mildly disruptive effect on synapse function and morphology, but is synergistically enhanced by simultaneous expression on both sides of the synapse (under the control of Scer\GAL4^A307).

Expression of Nrg^GPI.Scer\UAS in the giant fiber system throughout development (under the control of Scer\GAL4^A307) mimics the Nrg⁸⁴⁹ phenotypes; although essentially all giant fiber-tergo-trochanteral motor neuron (GF-TTMn) connections are physiologically disrupted, ~21% of the GF terminals appear to be anatomically normal at the light-microscopic level, whereas ~45% have thin synaptic terminals. A failure to extend a presynaptic terminal laterally in the second thoracic neuromere occurs in ~31% of the cases. Pathfinding defects in the brain are only rarely observed. Trans-synaptic fills between the GF and the TTMn are seen with less penetrance (only ~15% of the dye-injected GFs) compared to wild-type. Although the overall dendritic structure of TTMn is not affected by the expression of Nrg^GPI.Scer\UAS, large vesicles are occasionally observed in the medial TTMn dendrite.

Expression of Nrg^GPI.Scer\UAS through Scer\GAL4^A307 using the TARGET system during pathfinding has no effect on the giant synapse physiology in adults. The same treatment in a stabilized, mature synapse has only a mild effect on synapse function (eliciting 70%-80% wild-type responses). However, the presence of Nrg^GPI.Scer\UAS during nascent synapse formation elicits 30%-50% of the wild-type response, and during synapse formation elicits 25% of the wild-type response, while severely disrupting the GF-TTMn connection.

Pre- and postsynaptic expression of Nrg^GPI.Scer\UAS in the giant fiber system, under the control of Scer\GAL4^A307 results in the giant fibers either failing to increase their diameter, or to extend their presynaptic terminals laterally. While the gross anatomy of the tergo-trochanteral motor neuron (TTMn) is unaffected in Nrg^GPI.Scer\UAS (Scer\GAL4^A307) mutants, in about one-third of the preparations, abnormal large vesicles are observed in the medial dendrite.

Targeted expression of Nrg^GPI.Scer\UAS under the control of Scer\GAL4^Bx-MS1096 induces a number of axon guidance defects. Axons from the wing margin sensilla can also tangle and perforate the epithelial surface. At early stages of sensory axon extension, numerous ectopic contacts between axon and epithelium are seen.

Overexpression of Nrg^GPI.Scer\UAS in wing sensory neurons and two wing epithelial layers, mediated by Scer\GAL4^MS1075, causes a reduction in wing size and the appearance of ectopic sensory neurons. Additionally, there are severe axonal pathfinding defects including the distal extension of L1 axons, the absence of the proximal projection where the L1 and L3 nerve join in wild type, the clumping together of L1 axons and the penetration of the wing epithelium by the L1 nerve, an aberrant process which can extend beyond the wing tissue. Expression of Nrg^GPI.Scer\UAS under Scer\GAL4^MS1075 in a Nrg^l3 background results in the same phenotype.

Nrg^GPI.UAS, Nrg^l3, Scer\GAL4^MS1075 has wing phenotype, suppressible by Egfr[+]/Egfr^t1

Nrg^GPI.UAS, Scer\GAL4^MS1075 has wing phenotype, suppressible by Egfr[+]/Egfr^t1

Nrg^GPI.UAS, Scer\GAL4^MS1075 has wing phenotype, suppressible by Egfr^t1