Insertion at the first exon-intron junction.
Homozygous embryos hatch from the egg but never progress beyond first instar morphology and die within 7-10 days.
Homozygous stage 16 embryos show defects in the nervous system. Some embryos show a variability in the thickness of the commissures between different segments. The mutant embryos also show a loss of the separation between the two sets of longitudinal axons and weaker fasciculation of each of the six Fas2-positive bundles. No or few axons exit the central nervous system towards their peripheral targets. In the anterior of the embryo, most of the Fas2-positive axons appear to erroneously invade the brain rather than spreading out and innervating targets in the anterior periphery. The few axons that do target the periphery show various degrees of guidance defects. Similar defects are seen in the posterior of the embryo where most Fas2-positive bundles stop short of the posterior extent of the embryo.
Brfc07161, luteKG02251 has viable phenotype
Brfc07161, luteKG02251 has fertile phenotype
luteKG02251/Brfc07161 transheterozygous flies are morphologically normal, viable and fertile.
luteKG02251 fully complements Brfc07161.
Precise excision of the P{SUPor-P}luteKG02251 insertion reverts the lethal phenotype.