Rachelle Crosbie

email:  rcrosbie@physci.ucla.edu

phone:  (310) 794-2103

office:  2121 TLSB

homepage:  http://www.physci.ucla.edu/research/crosbie

research interests:  Inherited neuromuscular disease; muscular dystrophy

Research Interests

The goals of my research program are to (1) investigate the interaction and regulation of macromolecular adhesion complexes at the cell surface in normal and dystrophic skeletal and cardiac muscle, (2) elucidate the mechanisms that improve muscle cell adhesion to its surrounding extracellular matrix and govern muscle growth, and (3) use these basic discoveries to develop therapeutics that prevent muscle wasting. Our lab is focused on Duchenne muscular dystrophy, which is the most common lethal disorder of children. Genetic mutations in the dystrophin gene cause Duchenne muscular dystrophy, which is an X-linked disease that affects skeletal and cardiac muscle. We have discovered that the dystrophin associated protein, sarcospan, ameliorates muscle, cardiac, and respiratory dysfunction in mouse models of Duchenne muscular dystrophy. Sarcospan increases the expression of compensatory proteins that protect the muscle myofiber from contraction-induced injury. My lab is translating these results using pharmacological and genetic approaches that are expected to lead to advance our intellectual property filings and partnerships with pharmaceutical industries with programs in muscular dystrophy. In terms of my educational contributions, I have developed training programs in muscle cell biology and was recently awarded a NIH T32 training grant to support the program. I am Director of the T32 program, which supports graduate students and postdoctoral fellows. In addition, I am actively engaged in the Center for Duchenne Muscular Dystrophy at UCLA and the Senator Paul D. Wellstone Center of Excellence Partnership between Northwestern University, University of Florida, and UCLA. I serve as Director of the Wellstone Education Core at the UCLA site, which provides training for postdoctoral fellows. I have also been awarded grants from the UC Office of the President, in addition to grants from non-profit organizations to develop a new online course, PS121 "Disease Mechanisms and Therapies." Students at any of the UC ca

Selected Publications

Braddock, C. and Crosbie-Watson, R.H., "Education Innovation Task Force Report", 1-25 (2017) [link].

Gibbs, E.M. and Crosbie-Watson, R.H., "A simple and low-cost assay for measuring ambulation in mouse models of muscular dystrophy", J. Vis. Experiments, e56772 : 1-6 (2017) [link].

Gibbs, E.M., Marshall, J.L., Ma, E., Nguyen, T.M., Hong, G., Lam, J. Spencer, M.J., and Crosbie-Watson, R.H., "High levels of sarcospan are well tolerated and act as a sarcolemmal stabilizer to address skeletal muscle and pulmonary dysfunction i DMD", Hum. Mol. Genet, 25 : 5395-5406 (2016) [link].

Parvatiyar, M.S., Marshall, J.L., Nguyen, R.T., Jordan, M.C., Richardson, V.A., Roos, K.P., and Crosbie-Watson, R.H., "Sarcospan Regulates the Cardiac Hypertrophic Response and Prevents Cardiomyopathy Associated with Duchenne Muscular Dystrophy", J. Am. Heart Association, (2015) .

Marshall, J.L., Kwok, J., McMorran, B.J., Baum, L.G. and Crosbie-Watson, R.H., "The potential of sarcospan in adhesion complex replacement therapeutics for the treatment of muscular dystrophy", FEBS J, 280 : 4210-4229 (2013) [link].

Marshall, J.L. and Crosbie-Watson, R.H., "Sarcospan: a small protein with big potential for Duchenne muscular dystrophy", Skeletal Muscle, 3 (1): (2013) [link].

Rutkowshi, A., Bonneman, C., Brown, S., Thorsteinsdottir, S., Dominov, J., Ruegg, M.A., Matter, M., Guttridge, D., Crosbie-Watson, R.H., Kardon, G., Nagaraju, K., Girgenrath, M. and Burkin, D.J., "Report on the Myomatrix conference", Neuromuscl. Disord, 1-4 (2012) [link].

Marshall, J.L. and Crosbie-Watson, R.H., "Sarcospan: a small protein with large potential for Duchenne muscular dystrophy", Skeletal Muscle, (2012) .

Marshall, J.L., Chou, E., Oh, J., Kwok, A., Burkin, D.J. and Crosbie-Watson, R.H., "Dystrophin and utrophin expression requires sarcospan: loss of alpha 7 integrin exacerbates a newly discovered muscle phenotype in sarcospan-null mice", Hum. Mol. Genet, 21 : 4378-4393 (2012) [link].

Cabrera, P.V., Pang, M., Marshall, J.L., Kung, R., Nelson, S.F., Stalnaker, S.H., Wells, L., Crosbie-Watson, R.H. and Baum, L.G., "High-throughput screening for compounds that alter muscle cell glycosylation identifies new role for N-glycans in regulating sarcolemmal protein abundance and laminin binding", J. Biol. Chem, 287 : 22759-22770 (2012) [link].