11bp deletion beginning in the codon for I405. The frameshift results in the translation of 2 unique residues before a stop codon is reached.
Approximate endpoints of 11bp deletion reported as starting in codon I405. Deletions leads to frameshift and early translation termination.
NrtM54 is an enhancer of abnormal neuroanatomy phenotype of Scer\GAL4GMR.PF, msnEP549
Abl1/Df(3L)st-j7, NrtM54/NrtM2 has abnormal neuroanatomy phenotype
Abl4/Abl1, NrtM54 has abnormal neuroanatomy phenotype
Nrt[+]/NrtM54 is an enhancer of heart primordium phenotype of sli2
NrtM54 is an enhancer of photoreceptor cell & axon phenotype of Scer\GAL4GMR.PF, msnEP549
NrtM54/Abl1 is a suppressor of larval intersegmental nerve | heat sensitive phenotype of Nl1N-ts1
Nrt[+]/NrtM54 is a suppressor of larval intersegmental nerve | heat sensitive phenotype of Nl1N-ts1
Abl1/Df(3L)st-j7, NrtM54/NrtM2 has larval ventral nerve cord commissure phenotype
Abl4/Abl1, NrtM54 has larval ventral nerve cord commissure phenotype
The defects in photoreceptor cell projection patterns seen in larvae overexpressing msnEP549 under the control of Scer\GAL4GMR.PF are enhanced by NrtM54.
Heterozygotes of Df(1)N-8 or N55e11 with Abl1, NrtM54 or In(3L)std11 show defects in eye development leading to rough eyes with high penetrance.
Induced on: Abl1. The NrtM54 mutant allele was originally thought to be a mutation in the Dab gene (see FBrf0049327, FBrf0058531 and FBrf0084025), but sequencing of the chromosome indicates that it is a lesion in the Nrt gene.
"X ray" was stated as tentative. "ethyl methanesulfonate" was stated as tentative. Haploinsufficiency dependent upon an Abl mutant background (HDA).