Flashes delivered to ninaC⁵ mutant photoreceptors evoke a response with a slowly deactivating tail, with a time constant of approximately 200ms. When flash intensity is reduced to the level of single photons, the deactivation defect is reflected in the generation of multiple bump trains. These phenotypes are the same in Ca[2+]-containing and Ca[2+]-free solutions.

Illumination of ninaC⁵ mutant photoreceptors with orange light results in only partial internalisation of trpl^{ninaE.T:Avic\GFP-EGFP}.

Mutant flies have abnormal electroretinogram recordings; they show a much less pronounced acceleration of the rate of termination of the photoresponse by pre-exposure to light compared to wild-type flies, indicating a defect in long-term adaptation. Flies expressing ninaC^Δ132 in a ninaC⁵ background have a slower rate of termination of the photoresponse (measured using an electroretinogram recording) than wild-type flies after pre-exposure to light for 10 minutes.

The larval response to light is abolished in mutants (as measured by a "checker assay").

All rhabdomeres are completely degenerated in mutant photoreceptor cells.

Wild-type larvae reduce their path lengths and show increased head swinging when exposed to light. The reduced path length response is severely reduced, and the increased head swinging response is abolished in ninaC⁵ larvae. Wild-type larvae show a greater change in direction when lights are turned on or off (light (L) to dark (D), or D to L transition) than in the absence of a light transition (D to D). The amplitude of change of direction is greater for the D to L than for the L to D transition. This light-induced difference in the amplitude of change of direction for L to D and D to L transitions is abolished in ninaC⁵ larvae. The difference between the change of direction at the L to D transition and in the absence of a light transition (D to D) is not affected in ninaC⁵ larvae.

Like ninaC^Δ174, but unlike ninaC^Δ132, photoreceptors treated with 8-Br-cAMP or IBMX show no alteration in the kinetics of the macroscopic light response.

The electroretinogram response of homozygous flies is characterized by a larger corneal negative receptor potential in response to the first pulse of light than to subsequent pulses. Upon cessation of the light stimulus, the return to the dark state is slower in the mutant flies than in wild type.

Intracellular electrophysiological responses of ninaC⁵ photoreceptor cells are abnormal. Adaptation is reduced, resulting in the absence of the initial spike. Upon cessation of the light stimulus, the intracellular recording is typically characterised by an initial delay and an ensuing slow decline of the receptor potential.

Voltage clamped flash response shows delayed response termination. Plateau responses are also large in response to steady light. Also exhibits quantam bump-like activity in the dark and larger and longer bumps in the light. Turn-off to the pupil mechanisms is defective and the pupillary pigment migration is smaller than that in wild type.

ninaE¹⁷; ninaC⁵ double mutants exhibit degeneration of the outer and inner photoreceptor rhabdomeres and the intrusion of the rhabdomere membranes into the cell body.

ERG recording of the summed response of all retinal cells to light shows a large corneal negative response after a 90 second dark adaption, followed by a slow return to baseline and a small or absent off-transient upon cessation of the initial light stimulus.

Homozygous flies have an abnormal electroretinogram (ERG); the negative receptor potential produced in response to light is usually larger for the first pulse of light than for the second pulse of light, and the amplitude of the first response is usually larger than that of ninaC⁵ flies carrying ninaC^+t4.0. The amplitude of the off transient is greatly reduced, and the rate of return to the dark state is slower than normal. Rhabdomeres degenerate gradually in flies reared on a 12 hour light/12 hour dark cycle.

The axial cytoskeleton of the rhabdomeral microvilli is not detectable in newly eclosed ninaC⁵ flies. The number of multivesicular bodies in the photoreceptor cell cytoplasm is 3 times greater than wild-type.

Flies show light- and age-dependent retinal degeneration; non-photoreceptor cell degeneration is seen in young ninaC⁵ flies kept in the dark, while modest degeneration is seen immediately after eclosion in ninaC⁵ flies reared on a light-dark cycle. The diameter of the rhabdomeres is reduced by approximately 20% in these flies. The degeneration continues gradually, until the rhabdomeres are almost completely gone after 21 days. In some ommatidia the R7 rhabdomere is less degenerated than the six outer rhabdomeres. Flies reared in the dark for 21 days show a similar amount of degeneration as newly eclosed flies reared on a light/dark cycle. The diameter of the rhabdomeres of 21 day old, dark reared ninaC⁵ flies is reduced by approximately 25%. The decrease in prolonged depolarisation afterpotential seen in ninaC⁵ flies correlates with the amount of retinal degeneration. Young ninaC⁵ flies reared in the dark have an abnormal electroretinogram (ERG). The ERG of older light/dark reared ninaC⁵ flies is indistinguishable from the ERG of young, dark reared ninaC⁵ flies. The ERG of young, dark-reared ninaC⁵ flies carrying ninaC^+t11.2 is indistinguishable from wild-type. No retinal degeneration is seen in these flies after 21 days on a light/dark cycle.

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