Required for the maintenance of phospholipid turnover within the photoreceptor.

(UniProt, Q09103)

Photoreceptors degenerate during first week of adult life, although electroretinogram is small at time of eclosion when photoreceptors are morphologically normal; exception: rdg1 which is already aberrant then (Stark and Carlson, 1985); degeneration of outer photoreceptors (R1-6) in each eye facet is more severe (i.e., is essentially complete) than that of inner two cells (R7,8), with the most severe central-cell degeneration caused by rdgA1 and rdgA2, rdgA4 being less severe, and rdg3 still less (Harris and Stark, 1977); the ocelli degenerate, too, with rdgA1 causing particularly severe effect (Johnson et al., 1982); degeneration of compound eye photoreceptors is not light- or temperature-dependent (Harris and Stark, 1977); such degeneration is photoreceptor-autonomous in mosaics (Hotta and Benzer, 1970; Harris and Stark, 1977); degenerating photoreceptor axon terminals, especially those projecting from R1-6 into the lamina optic ganglion, are phagocytosed by glia in that optic lobe (Stark and Carlson, 1985); in general, though, the gross and internal structure of the lamina seems quite normal, even after photoreceptor degeneration caused by most severe rdgA alleles is complete (Meyerowitz and Kankel, 1978, Dev. Biol. 62: 112-42; Johnson et al., 1982; Stark and Carlson, 1985); two polypeptide spots in 2-d gel analysis of eye-specific proteins are reduced in intensity under influence of rdgA4 [Hotta, 1979, Mechanisms of Cell Change (Ebert and Okada, eds.). John Wiley, New York, pp. 169-82]; rdgA mutations said to cause hypoactive behavior, and one of them also leads to shaking on exposure to ether plus premature death after exposure to 29 (Homyk, Pye and Pak, 1981, Genetics 97: s50).