School of medicine

School Notes: School of Medicine
July/August 2014

Robert J. Alpern | http://medicine.yale.edu

Molecular biologist elected to the British academy

Joan Steitz, Sterling Professor of Molecular Biophysics and Biochemistry and a Howard Hughes Medical Institute investigator, was one of 60 scientists recently elected to the Royal Society, the United Kingdom’s national academy of science. Steitz was recognized for her pioneering work on the assembly of messenger RNAs—the molecules responsible for making proteins based on the instructions found in DNA. She is widely known for her discovery, with Michael Lerner, of small nuclear ribonucleoproteins, or snRNPs. These particles splice out the nonsense segments, called introns, of pre-mRNA, which must be removed before mRNA can build functioning proteins. 

An interim ophthalmology chair

Ron Adelman ’11MBA, professor of ophthalmology and visual science and director of the Yale Retina Service, will serve as interim chair of the Department of Ophthalmology and Visual Science, following the departure of James Tsai, who led the department since 2006. Adelman earned a master of public health degree from the University of California–Berkeley, completed residency training at Harvard Medical School and Stanford University School of Medicine, and completed a retina fellowship at the Massachusetts Eye and Ear Infirmary of Harvard Medical School. He also holds an MBA from Yale School of Management.

Finding the cause of metabolic syndrome

Yale researchers have contributed to the discovery of a single genetic mutation responsible for the myriad cardiovascular risk factors that comprise metabolic syndrome. In a study published May 15 in the New England Journal of Medicine, the group identified a mutation in individuals with metabolic syndrome in the gene Dyrk1B, a protein kinase involved in regulating the balance of muscle to fat and the stabilization of glucose levels. When mutated, the researchers found, Dyrk1B inhibited pathways that keep glucose levels stable, and “turned on” the pathways that promote the production of fat on the body. “Our findings suggest that mutation in genes that regulate the fate of these cells can result in more fat instead of muscle,” said senior author Arya Mani, associate professor of cardiology and genetics. Mani adds that animal studies suggest the activation of genes like Dyrk1B may actually increase appetite and cause weight gain. Therefore, because the gene is a protein kinase, which modifies other proteins, it may be a target for therapies that restore balance and reduce or eliminate the impact of the mutation.

The comment period has expired.