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Johns Hopkins Medicine
Office of Corporate Communications
Media Contact: Audrey Huang;
December 15, 2004
LOSS OF FRUIT FLY RETINA PROTEIN SPEEDS
BLINDING LIGHT DAMAGE
In experiments with fruit flies, Johns Hopkins researchers have found that blindness induced by constant light results directly from the loss of a key light-detecting protein, rather than from the overall death of cells in the retina, which in humans is a light-sensitive tissue at the back of the eye.
The research, reported in the Dec. 14 issue of Current Biology, overturns the long-standing belief that blindness from chronic light exposure is a direct result of overall retinal degeneration and cell death.
Although many animals, and presumably humans, lose both their retinal cells and vision after exposure to low levels of light for long periods, the relationship between exposure and blindness had been poorly understood.
In the Hopkins experiments, flies whose light-detecting protein rhodopsin was engineered to resist destruction retained their vision twice as long as normal flies, although over time they developed blindness due to delayed decay of rhodopsin. The researchers measured vision damage indirectly by measuring loss of the electrical signals normally initiated by rhodopsin when exposed to light.
"Everyone assumed that the blindness caused by chronic light exposure was an effect of the degeneration and loss of the retinal cells, but our experiments show these are two distinct events caused by two distinct processes," says Craig Montell, Ph.D., professor of biological chemistry in Hopkins' Institute for Basic Biomedical Sciences. "Understanding how degradation of rhodopsin and other visual proteins contributes to vision loss may help us in the future to reduce the severity of blindness in rare people susceptible to chronic exposure to light."
The light-detecting cells of fruit fly retinas share similarities with rod and cone cells of the human retina and also rely on rhodopsin to detect light and create an electrical signal that is transmitted to the brain.
In the researchers' experiments, this electrical signal was measured by a tool called an electroretinogram, which uses a contact placed on the surface of the eye. The measured signals get smaller as the flies lose their ability to see.
The researchers used the electroretinogram on normal fruit flies and found that these flies lost both their sight and some retinal cells after nine days of exposure, as expected. The researchers also found that rhodopsin levels were drastically lower after three days of exposure and virtually gone by day 13.
In genetically engineered flies whose rhodopsin destruction was inhibited in various ways, the researchers found no or relatively minor loss of the light-induced signal until much later. Other flies whose rhodopsin destruction had been genetically accelerated went blind twice as fast as normal flies. "We were quite surprised – we thought we'd prove correct what scientists had assumed was happening, but instead we proved that long-held idea wrong," says Montell.
Remarkably, the earliest vision loss in normal flies was reversible for up to three days of light exposure, says Montell. But after three days, when the eyes’ electrical signals were halved, the eyes reached a point of no return and vision never fully recovered. This point should be longer for other animals, since fruit flies' lifespan is only about 50 days.
The researchers are now searching for other proteins that reduce or prevent vision loss after exposure to constant light. They're also studying how constant light causes irreversible destruction of rhodopsin.
Authors on the paper are Seung-Jae Lee, Ph.D., and Montell from Hopkins. Lee is now a postdoctoral fellow in the Department of Biochemistry and Biophysics, University of California, San Francisco. This research was supported by a grant from the National Eye Institute.
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