At six days in light/dark cycles, Gαq1 mutants do not yet display appreciable signs of retinal degeneration. Gαq1 flies show substantial but much weaker electroretinogram response to light stimulation (even a very bright illumination) as compared to wild-type controls.
Gαq1 homozygous (and with a lower penetrance also heterozygous) third instar larvae display high frequency of ectopic targetting of type III axons to the abdominal body-wall muscle 13.
Gαq1 homozygous mutant late third instar larvae show impaired temperature selection and unlike controls display no strong preference for cooler temperatures (18[o]C) in a temperature gradient.
The gustatory aversion of mutant flies to 6mM camphor in a two way-choice test is not significantly different from that seen in wild-type flies.
Gα49B1/Gα49B961 adults show a defective electroretinogram response.
The minimum light intensity needed to induce a prolonged depolarization afterpotential is much lower than normal in mutant flies.
Mutants undergo slow light-dependent retinal degeneration.
The citronellal-evoked action potential frequency in ab12 basiconic sensilla in the antenna of mutant flies is not significantly different from wild type.
Mutant flies show significantly reduced avoidance of citronellal in a direct airborne repellent test (DART) assay.
ab11a olfactory receptor neurons (ORNs) in the antenna show a higher citronellal-evoked action potential frequency in mutant flies compared to in wild type.
Gα49B1 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).
Gα49B1 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.
The preference to choose 18[o]C over 24[o]C is greatly reduced in Gα49B1 mutants. Gα49B1 larvae are able to select 18[o]C over uncomfortably cool (14-16[o]C) and uncomfortably warm temperatures (26-32[o]C).
The rhabdomeres of 7 day old mutant flies have no obvious morphological changes relative to wild type.
Endocytosis of ninaE is normal in Gα49B1 photoreceptors.
At 10 days post eclosion, Gα49B1 retina exhibit smaller, disorganized and occasionally missing rhabdomeres relative to wild type. Gα49B1 flies raised in the light show significant retinal degeneration over 14 days, while Gα49B1 flies raised in the dark show little degeneration.
Gα49B1 has no significant effect on the visual impairment caused by exposure to constant light.
Mutant flies show no response to light (measured using an electroretinogram (ERG) recording).
Gα49B1 mutants do not exhibit the light dependent architectural changes seen in wild-type rhabdomeres.
Spontaneous quantum bumps of about 2pA in amplitude, which are detected in wild-type photoreceptors in complete darkness, are absent or greatly reduced in frequency in Gα49B1 photoreceptors. Gα49B1 photoreceptors show about a 1000-fold reduction in sensitivity to light compared to wild-type photoreceptors and mutant responses to brief light flashes decay abnormally slowly, returning to baseline with a time constant of about 100ms. The amplitude of light induced quantum bumps in the photoreceptors of Gα49B1 mutants are on average 3- to 4-fold smaller than wild-type, bump duration is reduced and the integral current is reduced about 5- to 6-fold compared to wild type (when ATP is present in the intracellular solution during recordings). When ATP is absent from the intracellular solution during recordings, the amplitude of quantum bumps from mutant photoreceptors increases to values approaching wild type.
The effect of anoxia as measured in the eye by extracellular voltage change recordings is similar to that of wild type except that the latency of onset of the larger phase of the response is twice as long as wild type.
Mutants raised in normal light show normal ommatidial structure and exhibit no loss of Deep pseudopupil.
Linolenic acid can activate light sensitive channels in mutant photoreceptors.
The size and shape of the quantum bumps are unaffected, although the frequency is significantly different from wild type.
Retina does not exhibit light-dependent degeneration. When present Gα49B1 is unable to suppress the retinal light-dependent degeneration of rdgC306 mutants.
Mutant photoreceptors show a dramatic loss of light responsiveness, displaying more than a 1000-fold loss in light sensitivity. Deactivation kinetics of the residual light response is very different from wild-type. Wild type has deactivation time constant of 19.0 +/- 5ms, compared to 127 +/- 24ms for mutant. Mutant photoreceptors display a dramatic decrease in the probability of quantum bump formation.