Visual pigment, sensitivity, and rhabdomere size were measured throughout a 12-h light/12-h dark cycle in Drosophila. Visual pigment and sensitivity were measured during subsequent constant darkness [dark/dark (D/D)]. MSP (microspectrophotometry) and the ERG (electroretinogram) revealed a cycling of visual pigment and sensitivity, respectively. A visual pigment decrease of 40% was noted at 4 h after light onset that recovered 2-4 h later in white-eyed (otherwise wild-type, wper + ) flies. The ERG sensitivity [in wper + flies in light/dark (L/D)] decreased by 75% at 4 h after light onset, more than expected if mediated by visual pigment (MSP) changes alone. ERG sensitivity begins decreasing 8 h before light onset while decreases in visual pigment begin 2 h after light onset. These cycles continue in constant darkness (D/D), suggesting a circadian rhythm. White-eyed period (per) mutants show similar cycles of visual pigment level and sensitivity in L/D; per's alterations, if any on the D/D cycles were subtle. The cross-sectional areas of rhabdomeres in wper + were measured using electron micrographic (EM) morphometry. Area changed little through the L/D cycle.
Between the two compound eyes on the vertex on the adult head are the three simple eyes, ocelli. Transmission and scanning electron microscopy were used to investigate the corneal lenses, ocellar photoreceptors, and axonal projections in normal and mutant Drosophila melanogaster. In wild type flies, the cornea consists of about 45 lamellae. It has corneal nipples distally and is underlaid with a monolayer of corneagenous cells. Retinula cells have open rhabdomeres of about 2 microns (diameter) x 7 microns (length). Rhabdomeres extend to the distal extent of the cell and do not have caps. Microvilli have a rodlet within. Retinula cells are joined by belt desmosomes on the lateral borders. Eye color pigment granules are housed within the retinula cells of normal flies, not in accessory cells. The granules do not migrate in response to light. No screening pigment granules exist in the white mutant. Each ocellus has about 80 retinula cells whose axons project to corresponding ganglia from which 4 giant afferent interneurons (per ganglion) project to the brain. receptor terminals are invested with capitate projections from glia. Receptors synapse onto dyads of follower cells, usually interneuron processes, at sites of T shaped presynaptic ribbons. These "T bars" are surrounded by indistinct flattened vesicles. Interneurons make feed back synapses onto receptor terminals at T bars clustered with distinct round vesicles. Three mutants with abnormal ocelli were investigated. The none mutant has unusual compound eye and ocellar corneas. The compound eye is devoid of differentiated photoreceptors but some axons from undifferentiated cells from synapses. No receptors were found in the ocelli of none. The oc mutant has no ocelli, although sometimes an ocellar cornea like that of none is seen; the compound eye is normal. The rdo mutant is also specific to ocelli with smaller ocelli having half the wild type allotment of receptor cells; the number of giant afferents is unaffected. Mutants best known for their compound eye defects were examined. The norpA mutant loses its ocellar rhabdomeres with age but has normal feed forward and feed back synapses. This normal synaptology prevails despite the electrophysiological defects in norpA ocelli reported earlier. The rdgABS12 mutant has poorly formed ocellar receptors which show some degeneration with age but synapses survive. The trp. rdgBKS222 and rgdAPC47 mutants are essentially normal with respect to structure and survival of ocellar receptors and synapses.
Visual receptor maintenance in Drosophila involves turnover of membrane. Coated pits derived from rhabdomere and plasmalemma, coated vesicles and multivesicular bodies (MVBs) of about 0.5 micron diameter characterize the early autophagic steps. Smaller electron dense bodies (0.15 micron) merge with MVBs. These are likely to be primary lysosomes as suggested by histochemistry for acid phosphatase in normal flies and an acid phosphatase deficient mutant. Aggregates of extracellular membranes confirm an earlier report that exocytotic shedding may also be employed in the fly with its open rhabdomeres. Microspectrophotometry was used to determine aspects of cycling of visual pigment to begin to correlate with what is known about membrane cycling at the ultrastructural level. Visual pigment decreases to about half 3 h after dawn then builds back gradually to maximum before dawn. Our fixations of tissue have been at the post-dawn period when autophagy may be high as inferred from visual pigment levels. In attempts to optimize our visualization of the constructive phase of the turnover process, we developed the paradigm of carotenoid 'replacement therapy'. Carotenoid replaced flies show an increase in visual pigment possibly associated with a streaming of membrane into the rhabdomere. Aged flies, studied to determine how effective maintenance is, have a unique accumulation of extracellular debris, and a small fraction of the receptors eventually degenerate.
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.
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