wing, with Nrgl3, Scer\GAL4MS1075
wing & sensory neuron | ectopic, with Scer\GAL4MS1075
wing vein L1 & wing nerve, with Scer\GAL4MS1075
wing vein L3 & wing nerve, with Scer\GAL4MS1075
Scer\GAL4MS1075-driven expression of Nrg167.Scer\UAS results in some weak alterations in ocellar sensory system axon guidance.
Overexpression of Nrg167.Scer\UAS in wing sensory neurons and two wing epithelial layers, mediated by Scer\GAL4MS1075, 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 Nrg167.Scer\UAS under Scer\GAL4MS1075 in a Nrgl3 background results in the same phenotype.
When Nrg180.I.Scer\UAS is driven by Scer\GAL4GMR.PF no effects are seen on the number of photoreceptor cells or cone cells present in the eye.
Nrg167.UAS, Scer\GAL4bun-GSG5961 has increased occurrence of cell division | adult stage phenotype, suppressible by EgfrDN.UAS.cBa, Scer\GAL4bun-GSG5961
Nrg167.UAS, Scer\GAL4bun-GSG5961 has adult posterior midgut epithelium phenotype, suppressible by EgfrDN.UAS.cBa, Scer\GAL4bun-GSG5961
Nrg167.UAS, Nrgl3, Scer\GAL4MS1075 has wing phenotype, suppressible by Egfr[+]/Egfrt1
Nrg167.UAS, Scer\GAL4MS1075 has wing phenotype, suppressible by Egfr[+]/Egfrt1
Nrg167.UAS, Scer\GAL4MS1075 has wing phenotype, suppressible by Egfrt1
Nrg167.UAS, Scer\GAL4GMR.PF is an enhancer of cone cell phenotype of Scer\GAL4GMR.PF, edUAS.cBa
Nrg167.UAS, Scer\GAL4GMR.PF is an enhancer of eye phenotype of Scer\GAL4GMR.PF, edUAS.cBa
Nrg167.UAS, Scer\GAL4GMR.PF is an enhancer of eye photoreceptor cell phenotype of Scer\GAL4GMR.PF, edUAS.cBa
The defective wing phenotype of Nrg167.Scer\UAS; Scer\GAL4MS1075 mutants is partially suppressed in a Egfrt1 or Egfrt1/+ background. Egfrt1 also suppresses the wing phenotype when Nrg167.Scer\UAS is expressed in a Nrgl3 background.
Nrg167.UAS/Scer\GAL4c316 partially rescues Nrgibx
Nrg167.UAS/Scer\GAL4Mef2.247 partially rescues Nrgibx
Nrg167.UAS/Scer\GAL4Ilp2.PR fails to rescue Nrg849
Nrg167.UAS/Scer\GAL430Y fails to rescue Nrgibx
Nrg167.UAS/Scer\GAL4Tab2-201Y fails to rescue Nrgibx
Nrg167.UAS/Scer\GAL4MS1075 fails to rescue Nrgl3
Expression of Nrg167.Scer\UAS under the control of Scer\GAL4c316 results in substantial rescue of the Nrgibx central brain phenotype.
Expression of Nrg167.Scer\UAS under the control of either Scer\GAL4Mef2.247, Scer\GAL430Y or Scer\GAL4Tab2-201Y does not appear to rescue the Nrgibx central brain phenotype.
Expression of Nrg167.Scer\UAS under the control of either Scer\GAL4Mef2.247 or Scer\GAL4c316 results in a significant increase in the sexual receptivity of Nrgibx females, while expression under the control of Scer\GAL4Tab2-201Y has no significant effect.
Expression of Nrg167.Scer\UAS under the control of Scer\GAL430Y results in a small but significant decrease in the sexual receptivity of Nrgibx females.
Scer\GAL4MS1075-driven expression of Nrg167.Scer\UAS in Nrgl3 mutant animals shows a synergistic increase in the expressivity of OP axon alterations (i.e. axonal alterations are much more severe in those individuals that display the phenotype).