Scott Wilson, Ph.D.
Primary Department Affiliation: Neurobiology
Primary Research Area: Neurodegeneration and Neurodegenerative Disorders
Learning, Memory, and Synaptic Plasticity
Neurodevelopment and Developmental Disabilities
Scott Wilson is an Assistant Professor in the Department of Neurobiology. Dr. Wilson received his B.S. degree in biology (1986) and his M.S. degree in microbiology (1989) from the University of South Florida. He then received his Ph.D. (1996) degree from the the Department of Molecular Genetics and Microbiology at University of Florida College of Medicine. He was a postdoctoral research fellow in the laboratory of Drs. Neal Copeland and Nancy Jenkins at the National Cancer Institute in Frederick, MD (1997-2002). His postdoctoral research focused on the genetics of neuro-degeneration in mice. He joined the Department of Neurobiology at UAB in 2002.
Research Interests: Mouse Models of Neuro-degeneration
The identification of genes involved in neuro-degeneration is a powerful means to understand the mechanisms of neuronal cell loss. Our laboratory focuses on identifying these genes through a variety of approaches in mice that include transgenics, gene-knockouts and positional cloning. We have recently cloned the mouse neurological mutation ataxia. The ataxia mouse displays a severe tremor and hind limb paralysis by 5 weeks of age. We showed that ataxia gene encodes Usp14, a member of the ubiquitin/proteosome pathway. During our analysis of the ataxia mouse, we found that loss of Usp14 results in synaptic transmission defects in both the central and peripherial nervous system. Since the members of this pathway act on a variety of substrates, we believe that the identification of the substrate(s) for Usp14 will provide important insights into the pathogenesis of the ataxia tremor and paralysis. In addition to Usp14, we are also investigating the function of several other members of the ubiquitin/proteosome pathway that are involved in neuronal function.
The mouse waltzer mutation is another mutation that we recently cloned. The waltzer gene encodes Cdh23, the newest member of the cadherin superfamily. Loss of this gene product in humans results in both auditory and vestibular dysfunction. We are currently producing antibodies and generating other alleles of Cdh23 to understand how this gene product functions in the perception of sound and maintenance of balance.
In addition to these projects, we are also in the process of identifying other spontaneous neurological mutations in mice. With the sequencing of the mouse genome, we are taking a candidate gene approach to identify the mutated genes in other neurological mice.