(Alliance, FBgn0003861 )

A light-sensitive calcium channel that is required for inositide-mediated Ca(2+) entry in the retina during phospholipase C (PLC)-mediated phototransduction. Ca(2+) influx may then feed back and inhibit PLC, thereby facilitating phosphatidylinositol 4,5 bisphosphate (PIP2) recycling. Trp and trpl act together in the light response, though it is unclear whether as heteromultimers or as distinct units, and are activated by fatty acids and metabolic stress. Also required for olfactory adaptation and may be involved in olfactory system development.

(UniProt, P19334)

Mutation believed to affect an intermediate step in phototransduction, the wild-type gene apparently encoding a protein involved in an intermediate step between photoreception and opening of the light-sensitive ion channels (Minke, 1977, 1982; Minke and Armon, 1980; Montell and Rubin, 1989; Suss et al., 1989). Although the mutants behave normally in dim light, they behave as though blind in bright light and there is an abnormally slow dark recovery (Cosens and Manning, 1969; Cosens, 1971). The light-evoked response of the photoreceptors, as shown in the ERG, decays to baseline during an intense, prolonged stimulus, but not during a dim or brief stimulus (Cosens and Manning, 1969; Minke et al., 1975); each quantum bump, however, seems intrinsically normal in shape and amplitude (Suss et al., 1989); fluoride ions, which lead to excitation and adaptation of wild-type photoreceptors in the dark when superfused onto an eye slice, did neither to mutant cells. A hydrolysis-resistant analogue of GTP, which excites wild-type photoreceptors and results in noisy depolarizations, reduced the mutant's light response. The visual pigment in R1-6 photoreceptors is normal in young trp flies, but its concentration decreases with age (Minke, 1982). The rhabdomeres degenerate with age and there is accumulation of glycogen granules (Cosens and Perry, 1972). Ultimately, photoreceptor cell bodies also degenerate (Isono, unpublished). Raising the mutant flies in complete darkness prevents the degenerative changes from appearing but has no effect on the electrophysiological phenotype (Isono and Pak, unpublished). Initially, the light-evoked migration of pigment granules occurs in a normal manner (i.e., toward the rhabdomeres) in trp mutants, but the granules move away after only five seconds of sustained light (Lo and Pak, 1981). The trp mutation (unlike norpA) does not block degeneration caused by rdgB (Chen and Stark, 1983, J. Insect Physiol. 29: 133-40); in a rdgB;trp genetic background, R1-6 photoreceptors are eliminated and the R7,8 photoreceptors that remain show the trp phenotype. trp is expressed in the photoreceptors of the ocelli as well as in those of the compound eyes (Hu et al., 1978; Montell et al., 1985). trp mutants seem to exhibit normal visually-mediated learning under the high light-intensity conditions that largely eliminate photoreceptor potentials (Reichert and Bicker, 1979).