Frontiers in Chemical Biology Seminar
Dr. He is the John T. Wilson Distinguished Service Professor in the Department of Chemistry and Department of Biochemistry and Molecular Biology at the University of Chicago. He received his bachelor of science degree in 1994 from the University of Science and Technology of China and his Ph.D. in chemistry from the Massachusetts Institute of Technology in 2000, studying under professor Stephen J. Lippard. After training as a Damon-Runyon postdoctoral fellow with professor Gregory L. Verdine at Harvard University, he joined the University of Chicago as an assistant professor, rising to associate professor in 2008 and full professor in 2010. He was selected as an investigator of the Howard Hughes Medical Institute in 2013. Dr. He’s research spans a broad range of fields including chemical biology, RNA biology, epigenetics, biochemistry, molecular biology, cell biology, and genomics. His recent research concerns reversible RNA and DNA methylation in biological regulation. His laboratory has spearheaded the development of enabling technologies to study the biology of 5-hydroxymethylcytosine (5hmC) in mammalian genomes. In 2011, his group discovered reversible RNA methylation as a new mechanism of gene expression regulation.
Over 150 types of post-transcriptional RNA modifications have been identified in all kingdoms of life. We have discovered the first two RNA demethylases, FTO and ALKBH5, which catalyze oxidative demethylation of the most prevalent modifications of mammalian messenger RNA (mRNA) and other nuclear RNA, N6-methyladenosine (m6A). These findings indicate that reversible RNA modification could impact biological regulation analogous to the well-known reversible DNA and histone chemical modifications. We have also characterized proteins that selectively recognize m6A-modified mRNA and affect the translation status and lifetime of the target mRNA, as well as molecular machines that deposit the m6A methylation on mRNA. Functional studies reveal m6A methylation as a critical mechanism to synchronize groups of transcripts for coordinated metabolism, translation, and decay, allowing timely and coordinated protein synthesis and transcriptome switching during cell differentiation and development. Misregulations of these processes lead to embryo lethality and human diseases such as cancer. I will present effects of m6A regulation on cancer progress and immune response.