Speaking fluent Minnesotan, Professor Peter Dedon began his scientific career with a BA degree in chemistry from St. Olaf College in Northfield, MN. He went on to earn MD and PhD degrees in pharmacology at the University of Rochester in 1987 and pursued postdoctoral research in chromatin biology at the University of Rochester and the chemical biology of DNA-cleaving anticancer drugs at Harvard Medical School. In 1991, Dedon joined the MIT faculty and helped create the Department of Biological Engineering in 1998. As an Underwood Prescott Professor in Biological Engineering, he is currently a PI in the SMART Infectious Disease group and a member of the MIT Center for Environmental Health Sciences, where he pursues research in infectious disease and inflammation.
With longstanding interests in the chemical etiology of human disease, his current research program emphasizes the chemical biology of RNA and DNA modifications in microbial pathogenesis and human cancer biology. His research group recently discovered phosphorothioate modifications in bacterial genomes, including the human microbiome, with these DNA modifications conferring resistance to oxidative stress. In collaboration with Tom Begley, his group used a systems-level analysis to discover a mechanism of translational control of cell response involving reprogramming of tRNA modifications and selective translation of codon-biased mRNAs for stress response proteins. This translational response mechanism has now been observed in eukaryotes, prokaryotes and even RNA viruses, with the discovery of a novel tumor suppressor mechanism and pathways controlling bacterial dormancy. The Dedon Lab currently collaborates with New England Biolabs in DNA modification discovery, Novartis Institute for Tropical Disease in dengue virus biology, Wuhan and Jiao Tong Universities in China in phosphorothioate chemical biology, NUS and NTU in Singapore in Pseudomonas, malaria, tuberculosis, dengue biology and drug development, and the Universities of Albany and Florida in mechanisms of translational control of cell response.