Scer\FRT-mediated recombination between the two progenitor insertions (PBac{WH}gsb-nf06670 and P{XP}gsb-nd07597) has resulted in a deletion between the 5'UTR and intron 3 of gsb-n, disrupting the entire open reading frame.
Scer\FRT-mediated recombination between the two progenitor insertions (PBac{WH}gsb-nf06670 and P{XP}gsb-nd07597) has resulted in a deletion between the 5'UTR and intron 3 of gsb-n.
Homozygous embryos show no obvious abnormalities in the SNa, ISN or ISNb motor axons.
Df(2R)GGGd13/+, gsb-ndel has lethal phenotype
Df(2R)gsbdb/+, gsb-ndel has lethal phenotype
Df(2R)gsbdb/+, gsb-ndel has abnormal neuroanatomy | embryonic stage phenotype
Df(2R)GGGd13/+, gsb-ndel has larval segmental nerve branch SNa of A1-7 phenotype
Two types of SNa axon defect are seen in embryos which carry gsb-nD-19A and are also transheterozygous for a deficiency removing both gsb-n and gsb (Df(2R)GGGd13): a 'thin' SNa phenotype, where the axons appear thinner but the normal bifurcation of the SNa is retained (75%) and a 'bifurcation missing' phenotype where the SNa axons lack the normal bifurcation and instead project inappropriately into the lateral muscle field (16%).