Amino acid replacement: R1419C.
C21575427T
R1467C | InR-PA; R1467C | InR-PB; R1467C | InR-PC; R1467C | InR-PD
R1419C
Mutation affects an active site residue, which mediates insulin receptor kinase substrate specificity.
Site of nucleic acid difference in mutant inferred by FlyBase based on reported amino acid change.
64% of homozygous female germline cysts are developmentally delayed. Mutant germline stem cells (GSCs) have a reduced division rate compared to wild-type GSCs. 1 in 6 egg chambers in mosaic ovarioles in which the entire germline is homozygous fail to progress through vitellogenesis.
InR353 mutants show no defects in opsin regulation.
In mosaic larvae in which homozygous clones have been induced in the eye, photoreceptor cell axons project normally through the optic stalk but fail to target the optic lobe properly. Mutant photoreceptor cell growth cones fail to expand at their termination points in the medulla. Surviving InR273/InR353 third instar larvae have guidance defects in the photoreceptor cell axons; gaps in the lamina, crossing of axons and failure of growth cone expansion in the medulla are seen.
InR05545/InR353, Tsc129 has partially lethal - majority live phenotype
Alleles of InR form an allelic series based on phenotypic strength: InR339 > InR31 > InR211 > InRE19 > InR353.
When in trans with Df(3R)e-D7 the lethal phenotype can be rescue by P{hs-inr}.