F1029I | cac-PA; F1029I | cac-PB; F1029I | cac-PC; F1029I | cac-PD; F1029I | cac-PE; F1029I | cac-PF; F1029I | cac-PG; F1029I | cac-PH; F1029I | cac-PI; F1029I | cac-PJ; F1029I | cac-PL; F1029I | cac-PM; F1135I | cac-PN; F1029I | cac-PO; F1029I | cac-PP
Amino acid replacement: F?I.
Transversion in the sequence encoding transmembrane domain IIIS6. This would be expected to affect all splice variants. The altered F residue is perfectly conserved in calcium channel α1 and sodium channel α subunits and some potassium channel subunits.
Nucleotide substitution: T?A.
GluRIIASP16/GluRIIASP16;cacS/+ third instar larvae show significant decreases in mEPSP (decreasing quantal size) and partial impairment of compensatory homeostatic increases in quantal content (significantly less quantal content than is seen in GluRIIASP16/GluRIIASP16 mutants alone but significantly more than wild type) at the NMJ. GluRIIASP16/GluRIIASP16 cacS/+ Cskj1D8/+ third instar larvae show significant decreases in mEPSP and quantal content at the NMJ.
One copy of CspDG29203 prevents the compensatory increase in quantal content seen in the NMJs of cacS/+; GluRIIASP16 mutant larvae that have reduced quantal size, resulting in impaired evoked neurotransmission. There is no increase in quantal content compared with cacS/+; CspDG29203/+ controls.
A cacS or cacS/cacNT27 background suppresses satellite frequency in sei2 mutants. Double mutants display a drastic decrease in both type B and M satellites, along with an even more pronounced reduction in the number of mature boutons and terminal branches.
The heterozygous cacS/+ mutation mildly suppresses, but does not abolish the synaptic homeostatic compensation response at the neuromuscular junction (NMJ) seen in homozygous GluRIIASP16 single mutants.
The recessive GluRIIASP16 single mutant NMJ synaptic homeostasis phenotype is completely suppressed in the presence of a heterozygous cacS mutation in combination with either an ExnEY01953 or an ExnEY-Δ23 heterozygous genetic background.
Extensive phenogenetic analysis of allelic combinations reveals a phenotypic series for visually mediated behaviors and genetically separable ERG defects and courtship song defects.