norpA7 mutants have no visual transduction in 90% of photoreceptor cells.
norpA7 mutant flies on 4 days of light exposure show retinal degeneration and loss of some photoreceptors; by 7 days of exposure they have undergone complete retinal degeneration with loss of most of the photoreceptors. No retinal degeneration is seen in dark-raised flies as compared to the WT control.
norpA7 mutants exposed to six days constant light display retinal degeneration. This degeneration is characterised by a decrease in rhabdomeres and disorganisation of the ommatidial array. Exposure to eight days of constant light leads to a complete loss of rhabdomeres.
After 4 weeks of constant light, norpA7 flies begin to exhibit signs of retinal degeneration. There is a decrease in the number of rhabdomeres with approximately 5 remaining per ommatidium. The rhabdomeres that remain are shrunken and exhibit vacuolization.
Mutant flies do not show defects in auditory responses, as measured by the sound-evoked compound action potentials in the antennal nerve and the displacement response of the antenna over a range of sound particle velocities.
norpA7 flies show a normal lifespan on dead yeast medium, but show reduced survival compared to controls on live yeast medium. The gut cells of the mutant flies fed on live yeast medium show severe apoptosis (the gut cells of mutant flies fed on dead yeast medium do not show severe apoptosis).
norpA7 flies show a 100-fold increase in the number of yeast colony-forming units (CFUs) in the gut compared to control flies when fed on live yeast medium.
norpA7 mutants exhibit greatly reduced thermotactic behaviour, losing the 18[o]C versus 24[o]C preference found in wild-type.
Mutant flies maintain a high level of activity in an open field arena over the full 10-minute assay (wild-type flies show a decay in locomotor activity over time in this assay).
norpA7 somatic mutant eye clones from animals raised in the dark and then exposed to 5 days of constant room light show massive retinal degeneration. These mutants exhibit loss of ommatidial organisation, and shrinking or disappearance of most of the rhabdomeres.
Electroretinograms show that, in contrast to controls, a light-stimulated change in the membrane potential of retinal photoreceptors is not observed in norpA7 flies.
By 21 days after eclosion, norpA7 flies display light-dependent retinal degeneration, characterized by irregularly shaped ommatidia with intracellular vacuoles and the loss of multiple photoreceptor cells.
Retinas from norpA7 mutant flies raised under continuous light conditions show no apparent retinal degeneration after 1 day, though degeneration (smaller rhabdomeres, some vacuolation) is evident by 6 days after eclosion.
norpA7 animals do not have a deep pseudopupil after 10 days in a normal light/dark cycle, indicating light-dependent retinal degeneration.
norpA7 animals have a normal heartbeat and response to serotonin or norepinephrine is normal.
After 6 days of exposure to continuous room light, norpA7 mutants exhibit a light dependant retinal degeneration phenotype. This is characterised by the phagocytosis of outer R1-R6 photoreceptor cell rhabdomeres by neighbouring cells.
The DHP-sensitive current is reduced. Application of TPA (phorbol 12-myrisatae 13-acetate) and PDD (phorbol 12,13-didecanoate), activators of PKC, rescues the current in mutant fibres without significantly affecting the normal current. 4αPDD (4α-phorbol 12,13-didecanoate), an inactive analog of PDD, does not affect the normal or mutant current. BIM (bisindolylmaleimide), an inhibitor of PKC, reduces the current in normal fibres without affecting the mutant current. DOG (sn-1,2-dioctanoyl-glycarol), analog of diacylglycerol increases the current in the mutant fibres.
The amplitude response to vapours of all odorants tested in the maxillary palp is not significantly different from wild type. The antennal response is also unaffected.
Males have red eyes. Flies are blind.
No difference in PIP2 levels, judged by its immunoreactivity, between light and dark adapted photoreceptors.
norpA7 partially suppresses the arrhythmicity of some homozygous e1 flies.
The major peak of phospholipase C activity seen in wild-type head extracts is missing from homozygous norpA7 head extracts.
Flies are blind. There is no receptor potential, and photoreceptors appear to degenerate relatively late in adult life.
The ocelli of 3 week old flies lack rhabdomeres, and there is an accumulation of debris under the cornea. The somata, projection and synapses of the receptor axons and interneurons appear normal, although occasionally abnormal striations on the soma's plasmalemma are seen.
norpA7 flies lack both the receptor potential and the transient components of the electroretinogram.
very small (<3mV) ERG, even with high intensity stimuli