Fly Guy: Biology Professor Earns 5-Year, $1.9M Grant to Study Dietary Impacts on Fly Eyes

Colleen Locke | Wed Jun 5, 2019

Research Could Lead to Preserving Human Eyesight

According to the World Health Organization, Vitamin A deprivation is the leading cause of preventable blindness in children. That’s why this spring Assistant Professor of Biology Jens Rister received a 5-year, $1,906,230 grant from the National Institutes of Health to study the effects of Vitamin A deprivation in the fly retina.

Rister, who this fall received the 2018 Endowed Faculty Career Development Award to support his work in understanding how the eye responds to a lack of Vitamin A, says he studies fruit flies, or Drosophila melanogaster, because flies don’t need Vitamin A to develop normally and deprived fly photoreceptors shrink, but do not die. In contrast, human photoreceptors die from lack of Vitamin A and can’t be regenerated. Rister therefore hypothesized that flies might have specific mechanisms that preserve vision under dietary stress.

In collaboration with Andrej Shevchenko, who studies proteins at the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden, Germany, Rister and his team recently discovered a novel protein that plays a key role in the response to Vitamin A deprivation and indeed stabilizes damaged photoreceptors: The deprived mutant flies showed severe anatomical, behavioral, and electrophysiological defects.

“This confirms our initial hypothesis that specific molecules respond to dietary stress to preserve vision. This also means that we potentially identified a novel signaling pathway,” Rister said.

Rister’s team also found that the novel protein targets the membrane of the light-sensing compartments of photoreceptors that lack vitamin A. Moreover, the protein also plays some sort of additional role in “normal” photoreceptor development when the deprivation isn’t taking place. Although they have some ideas, Rister’s team will be using the National Institutes of Health grant to figure out what this protein does in the two different contexts.

“Our approach combines genetics, transcriptomics, proteomics, electrophysiology, and behavioral analysis to delineate how photoreceptors respond to Vitamin A deprivation-induced damage and regenerate after vitamin A replacement therapy. It has the potential to identify novel molecular mechanisms that promote photoreceptor survival and could serve to treat human retinopathies,” Rister said.

Rister is also working with Roger Hardie of the University of Cambridge on this project.

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