rdgE1/Df(2R)vg135 transheterozygotes exhibit light-enhanced retinal degeneration; rapid retinal degeneration in light, after 5 days in a 12 hour light:dark cycle and a slower rate of degeneration when raised in constant darkness. Ommatidial arrangement is disorganised and rhabdomere size is reduced. rdgE1/Df(2R)vg135 transheterozygotes also exhibit photoreceptor degeneration which indirectly leads to the loss of the electrophysiological light response, the light response also decreases with age. TEM reveals the rdgE1/Df(2R)vg135 transheterozygotes exhibit abnormalities in rhabdomeric microvillar membrane stability and recycling causing random loss and vesiculation of rhabdomeres. rdgE1/Df(2R)vg135; ninaE17/ninaE17 double mutants exhibit small and abnormally shaped rhabdomeres, but lack the microvillar unpacking and vesiculation of the rhabdomere associated with rdgE1. One copy of norpA39 in rdgE1/Df(2R)vg135 transheterozygous males or females has only a slight effect at slowing the rdgE1-induced retinal degeneration.
Retinal degeneration phenotype. Degeneration begins two days post eclosion in constant light. This can be slowed in a 12h:12h light:dark cycle. Mutant flies with as yet undegenerated retina show a significantly decreased amplitude of light coincident response as measured by ERGs.
