Five different, well-characterized mutants of the R1-6 rhodopsin gene (ninaE), which corresponds to the rod opsin gene of vertebrates, have been examined morphologically as a function of age (up to 9 weeks) to determine whether or not the photoreceptors degenerate and to assess the pattern of degeneration. Structural deterioration of R1-6 photoreceptors with age has been found in all five mutants. The structural pattern of degeneration is similar in the five mutants, but the time course of degeneration is allele dependent and varies greatly among the five, with the strongest alleles causing the fastest degeneration. The degeneration appears to be independent of either the illumination cycle to which the animals are exposed or the presence of screening pigments in the eye. Although the degeneration first appears in R1-6 photoreceptors, eventually R7/8 photoreceptors, which correspond to cones of vertebrates, are also affected. In many of these mutants, striking proliferations of membrane processes have been observed in the subrhabdomeric region of R1-6 photoreceptors. It is hypothesized that (1) this accumulation of membranes may be caused by the failure of newly synthesized membranes that are inserted into the base of microvilli to be assembled into R1-6 rhabdomeres and (2) this failure may be caused by the extremely low concentration of normal R1-6 rhodopsin in the ninaE mutants.

The Drosophila mutant, oraJK84, lacks rhabdomeres in the major (R1-6) class of photoreceptors because these rhabdomeres rapidly degenerate in young flies. Genetic analysis reveals that oraJK84 actually contains two mutations (a ninaE and an ort allele) that affect the visual process. The mutation in ort appears to have no effect on photoreceptor structure. The other mutation occurs within the ninaE gene, which encodes the species of rhodopsin found in the R1-6 class of photoreceptors. Our analysis shows that this mutation is responsible for R1-6 rhabdomere degeneration in oraJK84 mutants. We also examined a ninaE mutant, denoted ninaEo117, that produces no ninaE transcript. The morphological phenotype observed in ninaEo117 is similar to that seen in oraJK84 mutants. We conclude that rhodopsin plays a vital role in maintaining photoreceptor structure in Drosophila.

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