The progenitor P{EP}HSPC300EP506 insertion remains on the chromosome. The 3' end of the insertion is flanked by a stretch of 208bp of HSPC300 sequences followed by an insertion of 208bp of unrelated sequences into the HSPC300 intron.
Homozygotes die at the late pupal stage.
Homozygous embryos (lacking zygotic HSPC300 function) have normal central nervous system axon morphology.
Homozygous embryos derived from homozygous female germline clones (lacking zygotic and maternal HSPC300 function) show severe, though variable, nervous system defects ranging from broken and disorganised longitudinal connectives and commissures to remnants of axons or depletion of all central nervous system axon bundles. In addition, lethality is shifted to embryonic stages in these animals and the embryos appear overall disorganised.
HSPC300EP506/HSPC300Δ54.3 animals show 30% viability.
Zygotic null, maternal hypomorph embryos (derived from HSPC300EP506/HSPC300Δ54.3 females mated to HSPC300Δ54.3/+ males) sometimes show abnormal crossing of the midline by axons (10% of embryos), and in the most severe cases, axons ectopically cross the midline several times. Commissures and longitudinal connectives are not properly formed.
The neuromuscular junctions of homozygous larvae are severely reduced in length (to 66% of wild type) and have supernumerary buds (88% increase compared to wild type). Heterozygous larvae also show a significant reduction in synaptic length compared to wild type.
Homozygous pharate adults occasionally have bent thoracic bristles, although the number of bristles on the head and thorax are normal.
HSPC300Δ54.3 is rescued by Scer\GAL4elav-C155/HSPC300UAS.cQa
HSPC300Δ54.3 is rescued by Scer\GAL4Act.PU/HSPC300UAS.cQa