Abstract:Because of the consequent lack of photopigment chromophore, carotenoid/ retinoid (vitamin A) deprivation during the larval period of Drosophila leads to decreased rhodopsin in adult photoreceptors. Decreased density of P-face particles in photoreceptor membrane (rhabdomeric microvilli) is a prominent ultrastructural feature of this rhodopsin deficiency. When adults are fed carotenoid, the rhabdomeric P-face particle density-which reflects the concentration of rhodopsin-increases halfway to the replete control … Show more
“…The Drosophila mutant outer rhabdomeres absent (ora) also has such membranes ; ora is an allele of ninaE (the Rl-6 opsin gene, see also below), hence the name ninaE ora (Washburn & OTousa, 1992). The site of zipper accumulation is directly confluent with rhabdomeric microvilli (Stark et al, 1992). Thus, the abnormality could reflect a defect of opsin deployment which results in a "storage disease."…”
In the δAsn20 Drosophila stock, the N-linked glycosylation site of opsin in Rl-6 receptors (Rhl) is absent. We used electroretinography (ERG), microspectrophotometry (MSP), and electron microscopy (EM) to quantify visual cell defects. Positive controls, w9, had wild type Rhl. MSP revealed minimal photopigment in δAsn20 for 6 days posteclosion; w9 had near normal visual pigment. ERG sensitivity and prolonged depolarizing afterpotential (PDA) were compared for δAsn20 and w9. δAsn20's Rl-6 function is decreased 100–fold at eclosion and diminishes until only R7/8 functions at 11 days. What little rhodopsin is routed to the rhabdomere functions. Morphometry showed smaller Rl-6 rhabdomeres in δAsn20 for 8 days posteclosion. Rhabdomeres in w9 were normal. A negative control, ninaE0117, a deletion of the Rhl gene, also has small rhabdomeres. δAsn20 and ninaE0117 lack the extreme rhabdomere elimination of ora (outer rhabdomeres absent), a nonsense mutant interrupting Rhl's coding sequence. δAsn20 and ora have surplus membrane while ninaE0117 does not. Freeze fracture reveals that δAsn20's rhabdomeric P-face particle count is as low as for vitamin A deprivation, consistent with an opsin defect. High particle density, organized into rows, is present in adjacent plasmalemma where surplus membrane accumulates. In summary, δAsn20 interferes with either synthesis, deployment, or maintenance of opsin.
“…The Drosophila mutant outer rhabdomeres absent (ora) also has such membranes ; ora is an allele of ninaE (the Rl-6 opsin gene, see also below), hence the name ninaE ora (Washburn & OTousa, 1992). The site of zipper accumulation is directly confluent with rhabdomeric microvilli (Stark et al, 1992). Thus, the abnormality could reflect a defect of opsin deployment which results in a "storage disease."…”
In the δAsn20 Drosophila stock, the N-linked glycosylation site of opsin in Rl-6 receptors (Rhl) is absent. We used electroretinography (ERG), microspectrophotometry (MSP), and electron microscopy (EM) to quantify visual cell defects. Positive controls, w9, had wild type Rhl. MSP revealed minimal photopigment in δAsn20 for 6 days posteclosion; w9 had near normal visual pigment. ERG sensitivity and prolonged depolarizing afterpotential (PDA) were compared for δAsn20 and w9. δAsn20's Rl-6 function is decreased 100–fold at eclosion and diminishes until only R7/8 functions at 11 days. What little rhodopsin is routed to the rhabdomere functions. Morphometry showed smaller Rl-6 rhabdomeres in δAsn20 for 8 days posteclosion. Rhabdomeres in w9 were normal. A negative control, ninaE0117, a deletion of the Rhl gene, also has small rhabdomeres. δAsn20 and ninaE0117 lack the extreme rhabdomere elimination of ora (outer rhabdomeres absent), a nonsense mutant interrupting Rhl's coding sequence. δAsn20 and ora have surplus membrane while ninaE0117 does not. Freeze fracture reveals that δAsn20's rhabdomeric P-face particle count is as low as for vitamin A deprivation, consistent with an opsin defect. High particle density, organized into rows, is present in adjacent plasmalemma where surplus membrane accumulates. In summary, δAsn20 interferes with either synthesis, deployment, or maintenance of opsin.
“…Previously, we had shown a decrease in visual sensitivity, visual pigment and P-face particle density in retinoid deprived Drosophila Stark, 1977 ;Stark, Ivanyshyn and Hu, 1976 ;Stark and Zitzmann, 1976) followed by fast recovery upon chromophore replacement (Chen and Stark, 1992 ;Sapp et al, 1991 ;Stark and White, 1996). Opsinpromoter-CAT-reporter analyses in Drosophila and Northern blot analyses in flies * For correspondence and reprint requests.…”
“…These turnover processes are controlled by ambient light conditions (Eguchi and Waterman, 1967;White, 1967;Blest et al, 1993;Blest and Stowe, 1997) though they are also modulated by factors such as the biological clock and the supply of material for rhodopsin biosynthesis (Barlow et al, 1980;White and Bennet, 1992;Ozaki et al, 1993;Huber et al, 1994;Stark and White, 1996).…”
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