Ultrastructure of the retina of Drosophila melanogaster: the mutant ora (outer rhabdomeres absent) and its inhibition of degeneration in rdgB (retinal degeneration-B).

The Drosophila mutant ora lacks rhodopsin in the R1-6 set of photoreceptors and has a diminution of the photopigment containing rhabdomeres of R1-6. Newly emerged flies have rhabdomeres, albeit small, which extend from the distal rhabdomere cap to the proximal basement membrane. As the fly ages, these are reduced until only distal remnants remain. Carotenoid deprivation does not protect ora flies from rhabdomere loss. When first characterized, ora was designated as a non-formation mutant rather than a degeneration mutant. The truth lies between, since rhabdomeres diminish with age but cells do not die. The plasmalemma of R1-6 have unusual dense striated areas like the "zippers" described earlier for the Drosophila mutant norpA. Similar membranes are also present within the receptor somata, especially in young flies. The latter probably become internalized from the plasmalemma. They are likely not related to the diminished rhabdomeres as claimed earlier. R7 and R8 have normal rhabdomeres, and in particular, they have normal coated vesicles and multivesicular bodies (MVB's), early steps in the degradation phase of normal rhabdomere maintenance. No MVB's are seen in the R1-6 somata, indicating that the routes for rhabdomere degradation differ from those of normal receptors. However, some MVB-like structures are seen in the intraommatidial cavity. The compound mutant rdgB;ora has a phenotype just like that of ora. This means that ora protects rdgB from the light induced degeneration of R1-6 which characterizes rdgB.