Peter Sudmant, PhD

The objective of my lab’s research is to understand how aging and age associated stresses impact molecular processes in different cell types, genetic backgrounds, and evolutionary contexts. We employ computational, statistical, and experimental methods to interrogate genetic and molecular phenotypic diversity at both the organismal and cellular level. In particular we are focused on studying processes of posttranscriptional gene regulation, somatic mutation, and genetic adaptation. These areas build upon wide ranging scientific contributions I have made to these and related fields over the course my PhD and Postdoc. My interests derive from a strong background in evolutionary genetics and genomics acquired over the course of my PhD at the University of Washington in the lab of Dr. Evan E. Eichler. Throughout my Ph.D., I worked to characterize genetic variants that differed between human populations and among great ape species. This work included one of the first characterizations of human duplicated gene family diversity (Sudmant et al 2010), as well as evolutionary analyses of structural variation in human populations world-wide (Sudmant et al 2015a, Sudmant et al 2015b). Over the course my PhD I authored and contributed to more than 20 peer-reviewed scientific publications, including 5 first-author publications, attesting to my work ethic and dedication, but also to my passion for science and my genuine interest in contributing to collaborative projects.

These publications and my PhD dissertation also span a diverse array of topics providing me with a rich understanding of the field of genetics. As a postdoctoral researcher in Dr. Chris Burge’s lab I studied post-transcriptional gene regulatory processes in the context of both evolution and aging. I resolved an ongoing controversy in evolutionary transcriptomics demonstrating how gene expression patterns among varying tissues differ among evolutionarily diverged organisms (Sudmant et al 2015c) and contributed new computational methods to the study of splicing dynamics (Taliaferro et al, 2016). I went on to discover a novel RNA species that accumulates in a cell type specific fashion in the aging brains of mice and humans, consisting of the 3′ UTRs of mRNAs absent their coding regions. I demonstrated that their mechanism of formation is through mRNA cleavage from impaired translational termination. This research identified a key role for stress-induced changes in ribosome dynamics in brain aging and discovered a novel RNA species associated with aging (Sudmant et a 2018).

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