April 23, 2009, Cambridge, MA --- The McGovern Institute for Brain Research at MIT will present the sixth annual Edward M. Scolnick Prize in Neuroscience to Jeremy Nathans, a Howard Hughes Medical Institute Investigator and professor of molecular biology and genetics, neuroscience, and opthalmology at Johns Hopkins University School of Medicine.
Dr. Nathans will deliver the Scolnick Prize lecture entitled "The Evolution of Trichromatic Color Vision" at the McGovern Institute on Monday, April 27, 2009 at 4 pm in the MIT Cognitive Sciences Complex, 43 Vassar Street (building 46, room 3002). The lecture, followed by a reception, is free and open to the public.
The Scolnick Prize is awarded annually by the McGovern Institute to recognize an individual who has made outstanding advances in the field of neuroscience. Nathans will receive the prize for his contributions to the understanding of color vision, brain development, and retinal disease.
"Jeremy Nathans exemplifies the spirit of discovery that we honor through this award," says Robert Desimone, director of the McGovern Institute and chair of the selection committee. "His pioneering work on the mechanism of color vision has led to an extraordinary range of insights into the function and development of the brain, as well as the basis for many forms of human blindness."
In work that he began when he was a graduate student, Nathans solved the mystery of the origin of human color blindness. Using his own DNA, he identified the genes for the three color-sensitive pigment proteins in the human retina. He showed that mutations in these genes cause can lead to different forms of color blindness, and that the red and green pigment genes are on the X-chromosome, which is why red-green color blindness is more common in men than women.
In addition to explaining the molecular basis of color vision, the discovery of these pigment proteins and the related protein rhodopsin was important because they are prototypes of a large family of proteins known as G-protein-coupled receptors. These proteins are key signaling molecules in all known organisms, and they represent the targets for about 1/3 of all FDA-approved drugs.
In more recent studies, Nathans and his colleagues discovered how genes control the normal development of the retina, and how defects in these genes disrupt the function and survival of retinal cells. These studies have revealed several defects that lead to human retinal diseases including Stargardt disease, the most common type of macular degeneration in children and young adults.
Nathans and colleagues also determined that the vitelliform type of macular dystrophy is caused by abnormalities in a member of a previously unknown family of ion channels proteins that allow ions to enter and exit cells.
|Contact: Julie Pryor|
McGovern Institute for Brain Research