In grnSPJ9/Df(3R)dsx3 mutants the intersegmental nerve (ISN) motor axons are stalled at muscles 2/10, leading to a near complete loss of innervation (~12-18%) of the dorsal-most muscles 1/9. In addition, grnSPJ9/Df(3R)dsx3 mutants display aberrant innervation of muscle 8. In affected hemisegments, a grossly normal pattern of axonal projections to the dorsal muscles 2/10 is observed, indicating that aCC and/or RP2, and at least one of the U motoneurons project aberrantly to muscle 8.
Shows a grn mutant phenotype. No abnormalities are seen when homozygous clones occupy the wing or distal leg segments. Clones on the proximal leg segments often severely affect the shape of the femur and tibia, which become shorter and broader than in wild type. In these cases the segments are approximately 1/3 shorter and 1/3 broader than normal, but leg segmentation is normal. The number of leg trichomes is normal.
Df(3R)dsx3/grnSPJ9 has abnormal neuroanatomy phenotype, suppressible | partially by Scer\GAL4eve.RN2/zfh1UAS.cPa
Df(3R)dsx3/grnSPJ9 has larval intersegmental nerve phenotype, suppressible | partially by Scer\GAL4eve.RN2/zfh1UAS.cPa
Expression of zfh1Scer\UAS.cPa in the aCC/RP2 neurons, under the control of Scer\GAL4eve.RN2 can only partially rescue the grnSPJ9/Df(3R)dsx3 motoneuron phenotype, with muscle 1/9 innervation increasing to 34% compared with the more severe (approximately 12%) grnSPJ9/Df(3R)dsx3 mutant phenotype.
Df(3R)dsx3/grnSPJ9 is rescued by Scer\GAL4eve.RN2/grnUAS.cBa
Df(3R)dsx3/grnSPJ9 is partially rescued by grnUAS.cBa/Scer\GAL4eve.CQ2
Expression of grnScer\UAS.cBa in the aCC/RP2 neurons, under the control of Scer\GAL4eve.RN2 efficiently rescues grnSPJ9/Df(3R)dsx3 mutant axon pathfinding (with 100% muscle 1/9 innervation). By contrast, expression of grnScer\UAS.cBa in the U motoneurons, under the control of Scer\GAL4eve.CQ2 only partially rescues the grnSPJ9/Df(3R)dsx3 mutant phenotypes, with approximately 54% of muscles 1/9 being innervated.
