Neurons in primary neuron cultures derived from mutant embryos have normal sized lamellipodia and normal length neurites.
Homozygous olfactory receptor neuron (ORN) clones show no defects in the axonal targeting pattern or number of Or59c-expressing ORNs.
9.7% of heterozygous border follicle cell clusters show defects in migration. Homozygous border follicle cells show defects in migration.
Tm1ZCL0722 is a suppressor | partially | somatic clone of abnormal neuroanatomy | somatic clone | adult stage phenotype of psidin55D4
Tm1ZCL0722 has border follicle cell | somatic clone phenotype, suppressible | partially | somatic clone by psidin55D4
Tm1ZCL0722 is a suppressor of lamellipodium phenotype of psidin55D4
Tm1ZCL0722 is a suppressor | partially | somatic clone of adult olfactory receptor neuron Or59c | somatic clone phenotype of psidin55D4
Tm1ZCL0722 is a suppressor | partially | somatic clone of border follicle cell | somatic clone phenotype of psidin55D4
The reduction in lamellipodia size and increase in neurite length which is seen in neurons in primary neuron cultures derived from psidin55D4 embryos are suppressed if the embryos are also mutant for Tm1ZCL0722.
psidin55D4 Tm1ZCL0722 double mutant Or59c olfactory receptor neuron (ORNs) show a marked reduction in the penetrance and severity of axonal targeting defects compared to psidin55D4 single mutant ORNs, but the reduction in the number of Or59c ORNs seen in psidin55D4 single mutant ORNs is not rescued in the double mutants.
Expression of psidinScer\UAS.cKa under the control of Scer\GAL4slbo.2.6 in a Tm1ZCL0722 heterozygous background results in border cell migration defects (45.1%).
Border follicle cells simultaneously homozygous for both Tm1ZCL0722 and psidin55D4 show less severe migration defects than single mutant border follicle cells.