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Microphotometric, ultrastructural, and electrophysiological analyses of light-dependent processes on visual receptors in white-eyed wild-type and norpA (noreceptor potential) mutant Drosophila

Published online by Cambridge University Press:  02 June 2009

Gregory M. Zinkl
Affiliation:
Millikin University, Decatur, Illinois
Linnette Maier
Affiliation:
Division of Biological Sciences, University of Missouri, Coloumbia
Kent Studer
Affiliation:
Division of Biological Sciences, University of Missouri, Coloumbia
Randall Sapp
Affiliation:
Division of Biological Sciences, University of Missouri, Coloumbia
De-Mao Chen
Affiliation:
Division of Biological Sciences, University of Missouri, Coloumbia
William S. Stark
Affiliation:
Division of Biological Sciences, University of Missouri, Coloumbia

Abstract

We examined a white-eyed strain of the norpA mutant (norpA;cn bw) and white (w)norpA+ controls using microspectrophotometry (MSP), electron microscopy (EM), and electroretinography (ERG). These studies revealed that light mediates receptor demise in norpA even though norpA lacks phototransduction. Rhodopsin and the rhabdomere which houses it decrease with increasing age in norpA but not in w with rearing on a 12 h light/12-h dark cycle or in constant light. At higher temperature in norpA;cn bw and w reared in constant light, visual pigment decreases, rhabdomeres diminish, and cells die. Importantly, dark rearing blocked visual pigment loss in norpA;cn bw; the M-potential, an ERG reflection of visual pigment level, corroborated this finding. MSP showed that norpA's visual pigment loss was not due to acute loss of metarhodopsin, rhodopsin's photoproduct. NorpA blocks certain processes expected to be light elicited. The alteration of visual pigment as a function of time of day, present in w controls, is absent in white-eyed norpA, suggesting that light-induced depolarization may be necessary to entrain the rhythm. Microspectrofluorometry using the fluorescent dye, Lucifer yellow, suggested that norpA lacks a light-induced uptake mechanism; using control flies, we determined the stimulus parameters required for uptake in vivo. An attempt to “cure” norpA;cn bw by replacement “therapy” using phospholipase C, missing in norpA's phototransduction cascade, was largely unsuccessful.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1990

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