Ora (outer rhabdomeres absent) is a nonsense mutation of rhodopsin **(Washburn & O'Tousa, 1989). **(Stark & Carlson, 1983) noted ³long convolutions and parallel arrays² of membrane that they supposed to be improperly exported pre-rhabdomeric membrane. **(Leonard et al, 1992) proposed a similar hypothesis about these membranes. Later, **(Stark & Sapp, 1987) speculated that these might be membranes being stripped from rhabdomeres, although they noted that they are also concentrated at cell junctions and in the plasmalemma. Such presumed massive shedding of rhabdomeres was present even in carotenoid deprived ora flies (Stark & Sapp, 1987). Importantly, (Stark & Sapp, 1987) show that retinula cells, even though they lack rhabdomeres, do not degenerate even out to 3.5 weeks, in contraction with the claims of **(Leonard et al, 1992) for the rhodopsin mutants they examined. **(Stark & Sapp, 1987) recognized a similarity with membranous ³zippers² described by **(Alawi et al, 1972) in norpA (no receptor potential) mutants.


The Stark lab also embarked on a line of research addressed to norpA (Stark et al, 1989A) (Stark & Sapp, 1989) where we noted the zippers that **(Alawi et al, 1972) first described. We were especially interested in a light-induced degeneration of norpA receptors (Zinkl et al, 1990) that had been discovered and characterized by Ostroy and coworkers (Ostroy, 1978) (Wilson & Ostroy, 1987) (Meyertholen et al, 1987). A formidable body of data, and a bewildering set of findings, was summarized thus: ³light mediates the need for upkeep by initiating rhabdomere autophagy or degradation of visual pigment; the excitation steps which culminate in depolarization and which are blocked by norpA are required for maintenance and renewal² (Zinkl et al, 1990).


The work in the Stark lab was turning to rhabdomere turnover (Stark et al, 1988). Membrane is presumably internalized from rhabdomeres (and the plasmalemma) at the site of coated pits that pinch off to coated vesicles. It is thought that the coated appearance is because of the protein clathrin. It was tempting to note the superficial similarity in the striped membranes of coated pits and the more extensive membranes seen in norpA and ora.


Stimulation by light was found to trigger uptake of fluorescent dye from the extracellular space into the photoreceptor cell in Drosophila (Wilcox & Franceschini, 1984). This finding was replicated but found to be deficient in norpA (no receptor potential) mutants (Zinkl et al, 1990); even though these flies lack the receptor potential, they still have light-induced rhodopsin-metarhodopsin interconversions. Are coated vesicles the site of light-mediated uptake?




Alawi AA, Jennings V, Grossfield J, Pak WL (1972) Phototransduction mutants of Drosophila melanongaster. The Visual System:  Neurophysiology, Biophysics, and Their Clinical Applications 24: 1-21


Leonard DS, Bowman VD, Ready DF, Pak WL (1992) Degeneration of photoreceptors in rhodopsin mutants of Drosophila. J Neurobiol 23: 605-626


Meyertholen EP, Stein PJ, Williams MA, Ostroy SE (1987) Studies of the Drosophila norpA phototransduction mutant. J Comp Phys 161: 793-798


Ostroy SE (1978) Characteristics of Drosophila rhodopsin in wild-type and norpA vision transduction mutants. J Gen Physiol 72: 717-732


Stark WS, Carlson SD (1983) Ultrastructure of the compound eye and first optic neuropile of the photoreceptor mutant oraJK84 of Drosophila. Cell Tiss Res 233: 305-317


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Zinkl G, Maier L, Studer K, Sapp R, Chen DM, Stark WS (1990) Microphotometric, ultrastructural and electrophysiological analyses of light dependent processes on visual receptors in white-eyed wild-type and norpA (no receptor potential) mutant Drosophila. Vis Neurosc 5: 429-439