Marie Burns, PhD, receives Cogan Award for unraveling mysteries of rod phototransduction deactivation

May 6, 2009

Marie Burns, PhD, received the Cogan Award for her work in retinal phototransduction. The award recognizes a young researcher who has made substantial contributions to work in ophthalmology or visual science directly related to ocular disorders and who also exhibits significant promise for future research. She is associate professor, Department of Ophthalmology and Visual Science, University of California-Davis.

Fort Lauderdale, FL-Marie Burns, PhD, received the Cogan Award for her work in retinal phototransduction. The award recognizes a young researcher who has made substantial contributions to work in ophthalmology or visual science directly related to ocular disorders and who also exhibits significant promise for future research. She is associate professor, Department of Ophthalmology and Visual Science, University of California-Davis.

She and her collaborators have been working on teasing out the secrets of the time course of signaling, specifically, the deactivation mechanisms of rod phototransduction.

“Deactivation is important because in a photoreceptor as long as the response of photon absorption persists, it interferes with the signaling generated from subsequent photon absorption,” Dr. Burns said. “We also believe that the photoreceptor is a wonderful model system for understanding the temporal regulation of G protein signaling in general.”

She explained that experiments on knockout rods have been enormously helpful in identifying the key players that are essential in normal photoresponse recovery.

“We know that rhodopsin has to be phosphorylated multiple times by rhodopsin kinase and after this arrestin binds with high affinity,” Dr. Burns said. “All of these steps have to occur on a high scale of the light response. We know that the RGS9/GB5/R9AP complex is essential to catalyze rapid GTP hydrolysis by Gα.”

The knockout experiments do not tell us the relative value of the rates of the reactions, however, she said. For these, we have to relay on changing the expression levels and concentrations in the living rods.

“Experiments suggest that rhodopsin deactivation is rapid in normal rats, about 50 milliseconds in normal rod, and that Gα/PDE activation is slow, about 200 milliseconds in normal rats, thus rate-limiting response recovery,” Dr. Burns concluded. “The Gα/PDE activation is dependent on the expression level of the RGS9 complex. This is interesting because it may be a mechanism that other G protein complexes use for tuning the overall duration of signaling.”