University of Minnesota
School of Physics & Astronomy

Biophysics Seminar

Wednesday, September 16th 2015
10:10 am:
Biophysics Seminar in 120 PAN
Speaker: Gant Luxton (Dept: Genetics, Cell Biology and Development, at UMN
Subject: Dystonia and Defective Nuclear-Cytoskeletal Coupling

The Luxton laboratory is focused on understanding the molecular mechanisms underlying the pathogenesis of dystonia. Dystonia is a neurological movement disorder characterized by repetitive muscle contractions that result in involuntary twisting of the extremities and abnormal posturing. People afflicted with dystonia can experience severe disruptions in their ability to perform routine tasks including walking and sitting. Dystonia is the third most common human movement disorder behind essential tremor and Parkinson’s disease. Despite its prevalence, we understand little about dystonia pathogenesis. The most common and severe form of inherited dystonia is early-onset or DYT1 dystonia. The symptoms of DYT1 dystonia first appear at a mean age of 12.5. DYT1 dystonia is caused by a mutation within the DYT1/Tor1a gene that encodes the evolutionarily conserved torsinA protein resulting in the deletion of a single glutamic acid residue (ΔE302/303, or ΔE). The mechanism through which the ΔE mutation causes DYT1 dystonia is unclear because the basic cellular function of torsinA is unknown. Our research has established torsinA as key regulator of nuclear-cytoskeletal coupling. We study the molecular mechanism of torsinA-dependent nuclear-cytoskeletal coupling using three powerful model systems: wounded fibroblast monolayers, the social amoeba Dictyostelium discoideum, and the Caenorhabditis elegans germline. Our research is holistic as we use biochemical, biophysical, cell biological, molecular genetic, and quantitative imaging approaches. Finally, we are actively screening for small molecules that modulate torsinA function in order to develop novel treatments for DYT1 dystonia.

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