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.
Studies synapse development and function relevant to human neuromuscular disorders.
The National Institute of Neurological Disorders and Stroke has awarded a $612,500 grant to Jackson Laboratory (JAX) Professor Robert...
Dr. Burgess is studying Charcot-Marie Tooth syndrome, a genetic neurological disorder that causes damage to the peripheral nerves, the...
New research provides an intriguing therapy target for some forms of Charcot-Marie-Tooth disease type 2.
Autism-spectrum disorders such as Asperger's syndrome, autism and Rett syndrome share certain characteristics, including...
The Jackson Laboratory has a large collection of mouse models of muscular dystrophy.
Researchers are coming up with associations between genes and disease states, but there are still very few proven causal...
C57BL/10ScSn-Dmdmdx/J mice (001801), commonly called mdx, are the most published model of Duchenne’s muscular dystrophy. The mice carry a...
D2.B10-Dmdmdx/J (013141) is a newer JAX strain created by backcrossing 001801 mice onto the DBA/2J background. This new strain better...
In the DyW strain (B6.129S1(Cg)-Lama2tm1Eeng/J, 013786), knock-out of the laminin alpha 2 gene models merosin-deficient congenital muscular...
Copy number variations (CNVs) can contribute to disease and other health issues.
JAX Professor Robert Burgess and collaborators are developing personalized gene therapy for a Texas child suffering from a neuromuscular...
Three studies published in Science (January 2016) successfully used CRISPR/Cas9-mediated genome editing in vivo to partially restore...
Muscle stem cells grown on an artificial scaffold in an optimized medium demonstrate preserved quiescence in vitro and enhanced...
Dmdmdx mutant mice, a model for Duchenne and Becker muscular dystrophy, are described.
Data from dystrophin (Dmd) and telomerase (Terc) double-deficient mice link shortened telomeres to increased disease...