A deletion resulting from the imprecise excision of P{EPgy2}ExnEY01953 removing a large portion of Exn.
Deletion resulting from the imprecise excsion of P{EPgy2}ExnEY01953. The endpoints were estimated from the graph and sequence in Figure 1. The second breakpoint is in an intron but the location within the intron was not reported.
Exn[+]/ExnEY-Δ23 is a non-enhancer of abnormal neurophysiology | third instar larval stage | recessive phenotype of GluRIIASP16
Exn[+]/ExnEY-Δ23 is a non-suppressor of abnormal neurophysiology | recessive | third instar larval stage phenotype of GluRIIASP16
ExnEY-Δ23, GluRIIASP16, cacS/cac[+] has abnormal neurophysiology | recessive | third instar larval stage phenotype
Exn[+]/ExnEY-Δ23 is a non-enhancer of embryonic/larval neuromuscular junction phenotype of GluRIIASP16
Exn[+]/ExnEY-Δ23 is a non-suppressor of embryonic/larval neuromuscular junction phenotype of GluRIIASP16
ExnEY-Δ23, GluRIIASP16 has NMJ bouton phenotype
ExnEY-Δ23, GluRIIASP16, cacS/cac[+] has embryonic/larval neuromuscular junction phenotype
GluRIIASP16 mutant larvae, also homozygous for an ExnEY-Δ23 allele, show a slight but significant increase in bouton number at the NMJ compared to GluRIIASP16 single mutants.
GluRIIASP16 mutant larvae, also homozygous for an ExnEY-Δ23 allele, show no difference in average active zone number per NMJ compared to GluRIIASP16 single mutants.
The recessive GluRIIASP16 single mutant NMJ synaptic homeostasis phenotype is not enhanced nor suppressed by a heterozygous ExnEY-Δ23 mutation.
The recessive GluRIIASP16 single mutant NMJ synaptic homeostatic response is completely suppressed in the presence of a heterozygous cacS/+ mutation in combination with an ExnEY-Δ23/+ heterozygous genetic background.
ExnEY-Δ23 is rescued by Scer\GAL4elav-C155/ExnUAS.EYFP
Presynaptic expression of ExnScer\UAS.T:Avic\GFP-EYFP driven by the pan-neuronal driver Scer\GAL4elav-C155 in a GluRIIASP16; ExnEY-Δ23 double mutant background is sufficient to fully rescue the ExnEY-Δ23 specific components in the abnormal neuromuscular junction synaptic homeostasis phenotypes associated with GluRIIASP16; ExnEY-Δ23 double mutants.