E989K | cac-PA; E989K | cac-PB; E989K | cac-PC; E989K | cac-PD; E989K | cac-PE; E989K | cac-PF; E989K | cac-PG; E989K | cac-PH; E989K | cac-PI; E989K | cac-PJ; E989K | cac-PL; E989K | cac-PM; E1095K | cac-PN; E989K | cac-PO; E989K | cac-PP; E989K | cac-PS; E989K | cac-PT; E989K | cac-PU
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
The loss of 'on' and 'off' transients in electroretinogram traces from cacF mutant clone cells in the eye of 3-day-old flies is suppressible by combination with cacGR-R1673P (the transients are actually larger than in controls) but not cacGR-R1664Q as compared to wild-type rescue flies (i.e. carrying Dp(1;3)DC131 for genomic rescue); the depolarization amplitude is comparable among all the various genotypes.
At 30 days of age, the transients loss is accompanied by decreased depolarization amplitude in cacF mosaic flies and either of these phenotypes can be significantly improved only by rescue with cacGR-R1664Q and not cacGR-R1673P.
The ultrastructural defects observed in cacF mutant photoreceptor cells at the level of lamina where they make connection with laminar neurons - expanded terminals, accumulation of autophagic vacuoles and signs of synaptic degeneration - are partially rescued in cacF;cacGR-R1664Q flies, but the neurodegeneration is further exacerbated in cacF;cacGR-R1673P flies.