Studies the molecular mechanisms of synapse formation, development and maintenance in peripheral neuromuscular junctions and retina.
The Burgess lab seeks to understand the molecular mechanisms of synapse formation and maintenance at two sites in the nervous system: the peripheral neuromuscular junction and the retina. In all of these studies, we are addressing basic molecular mechanisms, but these basic mechanisms have relevance to human neuromuscular and neurodevelopmental disorders. Our continued research on the genetics underlying these disorders, and our continuing effort to identify new genes involved in these processes, will increase our understanding of the molecules required to form and maintain synaptic connectivity in the nervous system.
11/96 - 08/01
Postdoctoral fellow, neurobiology
Washington University, St. Louis, MO
Stanford University, Stanford, CA
Michigan State University, East Lansing, MI
Professor, The Jackson Laboratory,
Bar Harbor, ME
Associate Professor of Medicine, Tufts University School of Medicine,
Associate Professor, The Jackson Laboratory,
Bar Harbor, ME
Assistant Professor, The Jackson Laboratory,
Bar Harbor, ME
Phi Beta Kappa
Outstanding Undergraduate Award,
Michigan State University Department of Biochemistry
Undergraduate Research Fellowship,
Michigan State University Honors College
Predoctoral Fellowship, National Science Foundation
Predoctoral Fellowship, National Institute of Mental Health
Morelli KH, Seburn KL, Schroeder DG, Spaulding EL, Dionne LA, Cox GA, Burgess RW. Severity of Demyelinating and Axonal Neuropathy Mouse Models Is Modified by Genes Affecting Structure and Function of Peripheral Nodes. Cell Rep. 18(13):3178-3191, 2017.
Spaulding EL, Sleigh JN, Morelli KH, Pinter MJ, Burgess RW, Seburn KL. Synaptic Deficits at Neuromuscular Junctions in Two Mouse Models of Charcot-Marie-Tooth Type 2d. J Neurosci. 36(11):3254-67, 2016.
Garrett AM, Tadenev AL, Hammond YT, Fuerst PG, Burgess RW. Replacing the PDZ-interacting C-termini of DSCAM and DSCAML1 with epitope tags causes different phenotypic severity in different cell populations. Elife. 5, 2016.
He W, Bai G, Zhou H, Wei N, White NM, Lauer J, Liu H, Shi Y, Dumitru CD, Lettieri K, Shubayev V, Jordanova A, Guergueltcheva V, Griffin PR, Burgess RW, Pfaff SL, Yang XL (2015) CMT2D neuropathy is linked to the neomorphic binding activity of glycyl-tRNA synthetase. Nature. 526:710-714, 2015.
Motley WW, Seburn KL, Nawaz MH, Miers KE, Cheng J, Antonellis A, Green ED, Talbot K, Yang XL, Fischbeck KH, Burgess RW (2011) Charcot-Marie-Tooth-Linked mutant GARS is toxic to peripheral neurons independent of wild-type GARS levels. PLoS Genet. 7:e1002399, 2011.
Fuerst PG, Bruce F, Tian M, Wei W, Elstrott J, Feller MB, Erskine L, Singer JH, Burgess RW (2009) DSCAM and DSCAML1 function in self-avoidance in multiple cell types in the developing mouse retina. Neuron. 64:484-497, 2009.
Fuerst PG, Koizumi A, Masland RH, Burgess RW (2008) Neurite arborization and mosaic spacing in the mouse retina require DSCAM. Nature. 451:470-474, 2008.
Seburn KL, Nangle LA, Cox GA, Schimmel P, Burgess RW (2006) An active dominant mutation of glycyl-tRNA synthetase causes neuropathy in a Charcot-Marie-Tooth 2D mouse model. Neuron. 51:715-726, 2006.