Pete Dedon is Underwood-Prescott Professor of Biological Engineering at the Massachusetts Institute of Technology. He is Lead Principal Investigator, Antimicrobial Resistance IRG, Singapore-MIT Alliance for Research and Technology, and a Member of the MIT Center for Environmental Health Sciences
Biography: Peter Dedon graduated with a B.A. in Chemistry from St. Olaf College in 1979, and an M.D. and a Ph.D. in Pharmacology from the University of Rochester in 1987. He 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 the Lead PI in the SMART Antimicrobial Resistance group and a member of the MIT Center for Environmental Health Sciences.
Research in the Dedon Lab focuses on the chemical biology of nucleic acids in three broad areas: epigenetics, epitranscriptomics, and genetic toxicology.
Pete’s lab is using analytical chemical techniques to study the ~20 DNA modifications that comprise the epigenome and the >140 chemical modifications of all forms of RNA (epitranscriptomics).
The Dedon Lab uses comparative genomics, single-molecule real-time sequencing, and mass spectrometry to discover novel DNA modifications, such as phosphorothioate and 7-deazaguanine modifications in bacterial and bacteriophage genomes. Work in bacteriophage points to a tremendous variety of DNA modifications with implications for biotechnology, synthetic biology, and human health and disease. For example, we have lab has found oxidation-sensitive phosphorothioate DNA modifications in 10-20% of the organisms in the human microbiome.
In the realm of the epitranscriptome, they applied systems-level analytics to discover a mechanism of translational modulation of gene expression common to humans, parasites, yeast, bacteria, and viruses. Here, environmental stressors cause a “reprogramming” of dozens of tRNA modifications to facilitate selective translation of codon-biased mRNAs critical to the cell stress response and survival, with families of stress-response genes defined by unique biases in the use of synonymous codons.
The Dedon Lab has had a long-standing interest in the chemical etiology of human disease, with a focus on the role of inflammation and endogenous DNA damage as drivers of carcinogenesis and age-related diseases. They developed a variety of analytical tools to interrogate genetic toxicology and endogenous molecular damage, including sensitive chromatography-coupled mass spectrometric methods to quantify dozens of different DNA, RNA, and protein damage products.
Learn more about Peter Dedon’s work on his lab website.