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

Abstract

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.

TRP, a protein essential for inositide-mediated Ca2+ influx is localized adjacent to the calcium stores in Drosophila photoreceptors

“…4B). Confirming the earlier studies in ninalP, the microvilli of Rl-R6 cells (but not R7) are &nificantly shorter relative to wild type (Stark and Sapp, 1987;Schinz et al, 1982;O'Tousa et al, 1989;Leonard et al, 1992). Furthermore, electron microscopy revealed two features that may be correlated with the increased expression of TRP protein in nind?…”

“…The life (Harris et al, 1976;Stark and Sapp, 1987; O'Tousa et al, ninuZ?% allele has no light-dependent receptor potential in Rl-1989;Leonard et al, 1992). Light microscopic immunostaining R6 cells (Harris et al, 1976;O'Tousa et al, 1989).…”

Dynamin- and Rab5-dependent endocytosis is required to preventDrosophilaphotoreceptor degeneration

“…Indeed, Rh1-containing MVBs have been reported during early phases of rhabdomere development, suggesting that the endocytic pathway could eventually exceed the rate of rhabdomeric membrane delivery during rhabdomere development (Satoh et al, 2005). On the other hand, the ninaE l17 mutant photoreceptors do not present MVBs (Stark and Sapp, 1987), a situation that is also observed upon interfering with Rab11 and Rab5 function (Satoh et al, 2005), and this is consistent with the idea that these MVBs are derived from rhabdomeric membrane. Altogether, this raises the possibility that by blocking Dynamin and/or Rab5 function in the photoreceptor, we are preventing MVB morphogenesis, a situation resulting in the accumulation of rhabdomeric membrane in the cell.…”

“…However, the molecular basis and, in particular, a link between such phenomena and the endocytic pathway is not clear. On the one hand, it has been proposed that rhabdomeric membrane turnover relies on the formation of coated pits and coated vesicles originating from the base of the rhabdomere and merging into MVBs (Sapp et al, 1991;Stark and Sapp, 1987). Indeed, Rh1-containing MVBs have been reported during early phases of rhabdomere development, suggesting that the endocytic pathway could eventually exceed the rate of rhabdomeric membrane delivery during rhabdomere development (Satoh et al, 2005).…”

Nir2, a Human Homolog of Drosophila melanogaster Retinal Degeneration B Protein, Is Essential for Cytokinesis

“…The first family member, the Drosophila retinal degeneration B (rdgB) protein, was cloned in 1991 by Vihtelic et al (56). Drosophila rdgB is implicated in the visual transduction cascade in flies, as rdgB mutant flies exhibit light-enhanced retinal degeneration and abnormal electroretinograms (16,18,45). More recently, four different mammalian genes similar to rdgB have been cloned by using different cloning strategies (1,5,14,26,28).…”