Mathematical Biology Program

University of Utah
Department of Mathematics

Mathematical Biology Program


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Mathematical Biology seminar

Kathleen Clark
Research Assistant Professor
Dept. of Biology and Huntman Cancer Institute
University of Utah
"Flies have muscle? Using flies to study human muscle disease"
April 21, 2004 3:05pm in LCB 215

Abstract: Muscle cells respond to increased demand for work output by growth and remodeling. This indicates that muscles have a biomechanical sensor that can detect changes in muscle stretch, and direct changes in gene expression and cellular organization. Mutations in proteins important for sensor function would impair the growth/remodeling process, leading to muscle failure. Stretch and other forms of mechanical stress are likely sensed at anchor points present in the contractile apparatus; when muscle contracts or is stretched, these anchor points are the main conduits of the mechanical forces produced. Thus, proteins present at these sites may be components of the biomechanical sensor. We are studying proteins that have features suggestive of a function in the biomechanical sensor. One of these proteins - Muscle LIM protein (MLP), is present at the anchor sites, but can also be found in the nucleus, suggesting that it might shuttle between these two cellular compartments, to convey information from the sensor to the nucleus. In fact, mutations in MLP lead to dilated cardiomyopathy and hypertrophic cardiomyopathy - two forms of heart failure that result from aberrant remodeling of the heart. We are using the genetics system of the fruit fly, Drosophila melanogaster, to test specific hypotheses about MLP function. For example, we are testing whether MLP needs to be able to reside in the nucleus in order to function. In addition, we can take advantage of the genetic tools available in the fly to find other proteins that function with MLP. This information will help us to determine the molecular pathway in which MLP acts. Using these types of experiments, we hope to confirm that MLP is part of the biomechanical sensor, and moves into the nucleus in response to increased muscle load. In addition, we should be able to identify other components of the sensor, which may represent uncharacterized mutations responsible for cardiomyopathies.

For more information contact J. Keener, 1-6089