neuromuscular junction & synapse
SCARΔ37/+;trio123.4/+ or SCARΔ37/+;AbiKO/+ double heterozygous embryos show stalling of the ISNb motor nerve at the junction of muscles 6 and 13 with failure to innervate muscle 12 in 51% and 79% of examined hemisegments, respectively - a strongly increased penetrance compared to any of the single heterozygotes.
SCARΔ37/+ partially suppresses the embryonic lethality and dorsal closure defects seen in embryos expressing crbY10A in a crbGX24w-/crbGX24w- background, resulting in some adults surviving, although these adults show defects in abdominal development.
SCARΔ37;Vrp1f06715 double homozygous mutant embryos show normal gut constriction but aberrant morphology. Longitudinal visceral muscle founder cells show aberrant migration and severe muscle fusion defects are observed: mostly mononucleated and binucleated muscle cells are seen at late embryonic stages. These defects are weaker in SCARΔ37/SCARΔ37;Vrp1f06715/+ embryos (founder cell migration mostly normal though fusion defects are still observed) and not much improved in SCARΔ37/+;Vrp1f06715/Vrp1f06715 embryos (both founder cell migration and muscle fusion defects observed).
A SCARΔ37 heterozygous mutant background enhances the actin remodelling and subsequent basolateral invasion of epithelial cells seen in flies expressing CskGD9345 in a stripe of cells at the anterior/posterior boundary of the larval wing disc under the control of Scer\GAL4ptc-559.1.
One copy of SCARΔ37 partially suppresses the cuticle defects seen in α-Cat1 mutant embryos. Embryos show less severe defects on average and a fraction of embryos have normal heads. The phenotype is more severe when SCARΔ37 is introduced maternally rather than paternally.
A SCARΔ37 heterozygous background enhances the patterning defects found in Scer\GAL4GMR.PF>cindrdsRNA.PC.PD.Scer\UAS mutants. The mean interommatidial precursor cell number and the number of cone and/or 1[o] cell errors is increased in these double mutants.