Amino acid replacement: ?270term.
Mutation is the second PDZ domain.
Nucleotide substitution: ?811?.
C22857286T
?811?
Q271term | inaD-PA; Q283term | inaD-PB
?270term
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
Compound action potentials can be evoked by sound in the antennal nerve of mutant flies, but the sound particle velocities required to elicit the response is increased compared to wild type. The displacement response of the antenna over a range of sound particle velocities is linearised, indicating loss of mechanical amplification.
The photoreceptors of newly eclosed flies expressing inaDninaE.T669A in a inaDT1 mutant background show a slower response to brief (1ms) flashes containing ~75 effectively absorbed photons. Peak amplitude is similar to wild type but the time to peak is delayed and the decay time course is slower. Following 1s light steps of increasing intensity wild type responses consist of an initial peak that rapidly declines to minimum (the "notch"); this "notch" is more pronounced in inaDT1 inaDninaE.T669A mutant flies. Although the intensity dependence of both the peak and plateau in mutants are indistinguishable from wild-type, the "notch" develops at 2-3 fold lower intensities than in controls.
The light-triggered translocation of trplninaE.T:Avic\GFP-EGFP is abolished in inaDT1 flies.
Inhibition of trplninaE.T:Avic\GFP-EGFP internalisation is observed in inaDT1 mutant photoreceptors.
Mutants have single photon responses that are grossly disorganised, with large defects in amplitude, latency and deactivation. Quantum bumps have amplitudes less than one fifth of those of controls, latencies that are roughly six times greater than wild type and responses that fail to terminate normally, with single photons producing several microbumps. Double mutants with of Camunspecified with inaDT1 show a noisy, continuous response to a single photon of light, and do not produce individual bumps.
inaDT1 flies have an abnormal electroretinogram (ERG) phenotype, with severe defects in response to light. Loss of responsiveness to light increases with age.
inaDT1 is a suppressor of rhabdomere phenotype of rdgA1
inaDT1/inaDsu1 is a suppressor of rhabdomere phenotype of rdgA1
inaDsu100/inaDT1 is a suppressor of rhabdomere phenotype of rdgA1
inaDT1 is rescued by inaDninaE.PM
inaDT1 is partially rescued by inaDGMR.GFP
inaDT1 is partially rescued by inaDC645S.ninaE
inaDGMR.T:Avic\GFP rescues the electroretinogram response of inaDT1 flies to near wild type.
Light-raised inaDttd10 in trans with inaDT1 shows partial translocation of trplninaE.T:Avic\GFP-EGFP from the rhabdomere to the cell body. It should be noted that the trplninaE.T:Avic\GFP-EGFP translocation defect in homozygous inaDttd10 mutants is more severe than in trans with inaDT1. inaDttd10/inaDT1 flies exhibit almost normal internalisation in some photoreceptor cells of each ommatidium whereas the internalisation defect is observed in all photoreceptor cells in homozygous inaDttd10 mutants.