Excision of the P{PZ} element, deleting the transcription unit.
Defasciculation of the normally tightly associated ocellar pioneer axons is seen in 70% of homozygous pupae and in 66% of Nrt1/Nrt5 pupae before head eversion. Axons of the ocellar and postvertical mechanoreceptors leave the epidermal surface and associate with the ocellar pioneer nerve in 50% of pupae expressing NrtScer\UAS.cSa under the control of Scer\GAL4Mz1407 in an Nrt5 background. Wing vein sensilla frequently have axons that turn back toward axons of the triple row, creating a loop that prevents both types of axons from leaving the wing in the direction of the central nervous system. Axons of the ocellar and postvertical mechanoreceptors leave the epidermal surface and associate with the ocellar pioneer nerve in 53% of pupae expressing NrtScer\UAS.cSa under the control of Scer\GAL4sca-537.4 in an Nrt5 background. In 16% of pupae before head eversion both sides of the head capsule come closer together than normal due to a fold along the midline of the head. Wing vein sensilla frequently have axons that turn back toward axons of the triple row, creating a loop that prevents both types of axons from leaving the wing in the direction of the central nervous system. Homozygous embryos show a slightly delayed axogenesis, a lack of nerve cord condensation that persists post-embryonically and a mild constriction of the nerve cord. Fas2 expressing axons sometimes show defects in homozygous embryos, including stalling or misrouting of axons. Fas2 expressing axons sometimes show defects in Nrt1/Nrt5 embryos, including stalling or misrouting of axons.
Nrt5 has larval longitudinal connective phenotype, enhanceable by Nrgl4
Nrt5 has symmetrical commissure phenotype, enhanceable by Nrgl4
Nrt5 has dMP2 neuron phenotype, enhanceable by Nrgl4
Nrt5 has larval MP1 neuron phenotype, enhanceable by Nrgl4
Nrt5 has SP1 neuron phenotype, enhanceable by Nrgl4
Nrt5, kek1RM2 has axon | embryonic stage phenotype
Nrt5, drlP3.765 has axon | embryonic stage phenotype
Nrt5, kek1RA5/kek1RM2 has axon | embryonic stage phenotype
Nrt5, kek1RA5 has axon | embryonic stage phenotype
The frequency of axons showing defects is increased if the embryos are also homozygous for Nrgl7. Nrgl4 Nrt5 double mutant embryos have a severe CNS phenotype, with thinning or complete interruption of the longitudinal connectives, and fusion of the commissures. Defects in Fas2 expressing neurons similar to those seen in Nrt5 single mutants are seen, although with much higher expressivity and penetrance. Axons of the dMP2 and MP1 neurons either stall or delay their extension considerably in 29% of cases. The ventral unpaired medial (VUM) neurons show misguidance phenotypes in 15% of cases, and anomalies in the trajectory of the SP1 axon are observed rarely. The pCC and vMP2 axons grow normally in most hemisegments, and the aCC and U neurons are normal. These defects are rescued by NrtScer\UAS.cSa expressed under the control of Scer\GAL4Mz1277. The frequency of axons showing defects in Nrt1/Nrt5 embryos is increased if the embryos are also homozygous for Nrgl4 or Nrgl7. drlP3.765/drlP3.765; Nrt5/Nrt5 and drlP3.765/Df(2L)TW130 ; Nrt5/Nrt5 embryos show strong misguidance and stalling phenotypes in many hemisegments of axons that normally express drl. In addition, similar defects are seen in axons that do not normally express drl. Defects in Fas2 expressing axons, associated with the defects in drl expressing axons are also seen. These defects are rescued by NrtScer\UAS.cSa expressed under the control of Scer\GAL4Mz1277. Extension of longitudinal axons through the intercommissural region is frequently abnormal in kek1RM2; Nrt5 and kek1RA5/kek1RM2 ; Nrt5 embryos. In addition, Fas2 expressing axons show defasciculation, stalling and guidance defects, including crossing of the midline.
Nrt5 is partially rescued by NrtUAS.cSa/Scer\GAL4sca-537.4
Nrt5 is not rescued by Scer\GAL4insc-Mz1407/NrtUAS.cSa
The ocellar pioneer axon phenotype is not rescued by NrtScer\UAS.cSa expressed under the control of Scer\GAL4Mz1407, and is partially rescued by NrtScer\UAS.cSa expressed under the control of Scer\GAL4sca-537.4. The stalling and misguidance phenotypes can be rescued by NrtScer\UAS.cSa expressed under the control of Scer\GAL4Mz1277.
