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Douglas M. Swank
Assistant Professor, Department of Biology
Rensselaer Polytechnic Institute
Education:
Ph.D., Physiology, University of Pennsylvania, 1995
B.A., Biology, Magna Cum Laude, University of Rochester, 1990
Career Highlights:
Swank joined the Rensselaer biology faculty in the fall of 2005, after completing his work as a research associate in the Department of Molecular Physiology and Biophysics at the University of Vermont College of Medicine. Prior to his role in Vermont, he spent four years as a postdoctoral fellow in San Diego State University’s Department of Biology. The American Heart Association (AHA) and the National Institutes of Health (NIH) provided funding for his studies. His previous experience also includes serving as a research assistant at the State University of New York (SUNY) Buffalo in both the physiology and molecular biology departments.
Among the honors Swank has received are an R03 Award, NIH, 2004; the Porter Award, Society of General Physiologists, 2001; Caroline Suden/Francis Hellebrandt Professional Opportunity Award, the American Physiological Society (APS), 2000; Clifford and Evelyn Cherry Postdoctoral Research Award, AHA, 1999; and the Procter & Gamble Professional Opportunity Award, APS, 1995.
Swank’s professional contributions include serving as co-chair of Biophysical Society Meeting platform sessions for two years, and presenting invited seminars at universities such as Pennsylvania State University and University of California, Berkeley. He also serves as an ad hoc grant reviewer for the National Science Foundation and the Biotechnology and Biological Sciences Research Council in the United Kingdom. His professional memberships include APS, Biophysical Society, American Association for the Advancement of Science, American Society of Cell Biology, Phi Beta Kappa, and Sigma Xi.
Research Areas:
Swank’s laboratory investigates how muscle is designed to perform an amazingly wide variety of tasks including locomotion, pumping blood, and sound production. These studies involve Drosophila, mice, fish, and other organisms likely to reveal novel insights into muscle performance. One aspect of this research is to better understand muscle disease states such as familial hypertrophic cardiomyopathy (FHC). FHC is an inherited genetic disease that is a major cause of sudden death among young adults.
His laboratory’s primary focus is to determine how variation between muscle fiber types (e.g. slow- versus fast-contracting fibers) is generated. An integrative approach is taken, starting with muscle genes such as myosin, and moving up in scale to protein expression and function, muscle mechanics, and whole organism studies. This comprehensive approach is possible by exploiting the unique genetic properties and transgenic techniques available with Drosophila. Drosophila is currently the only system that can be transgenically manipulated to express a specific myosin isoform or mutant myosin in a specific muscle type. The expressed myosin can be isolated from Drosophila to measure single and ensemble biochemical and biophysical molecular properties such as ATPase rates, actin sliding velocity and myosin step size. Laboratory members also measure mechanical properties (e.g. power, velocity and force) of isolated muscle fibers expressing transgenic myosin and relate altered fiber properties to observed changes in locomotion, such as flight ability.
Some of the myosin structural regions Swank is investigating using Drosophila (e.g. the “converter” region) are hot spots for point mutations that lead to FHC. He is also directly studying the effects of these mutations on cardiac muscle performance using transgenic mouse models of FHC. Besides myosin, the laboratory also investigates the function of other muscle proteins such as muscle LIM protein (MLP), actin, and paramyosin.
Selected Publications:
D.M. Swank, W.A. Kronert, S.I. Bernstein, and D.W. Maughan, “Alternative N-Terminal Regions of Drosophila Myosin Heavy Chain Tune Muscle Kinetics for Optimal Power Output,” Biophysical Journal, in press.
D.M. Swank and J.O. Vigoreaux, “The Development of the Flight and Leg Muscle,” in Comprehensive Molecular Insect Science, L.I. Gilbert, K. Iantrou, and S. Gill, eds., Elsevier Science Ltd., Oxford, UK., in press.
K.M. Littlefield, D.M. Swank, B. Sanchez, A.F. Knowles, D.M. Warshaw, and S.I. Bernstein, “The Converter Domain Modulates the Kinetic Properties of Drosophila Myosin,” American Journal of Physiology, 284, (4), C1031-C1038, (2003).
D.M. Swank, A.F. Knowles, W.A. Kronert, J.A. Suggs, G.E. Morrill, M. Nikkoy, G.G. Manipon, and S.I. Bernstein, “Variable N-Terminal Regions of Muscle Myosin Heavy Chain Modulate ATPase Rate and Actin Sliding Velocity,” Journal of Biological Chemistry, 278, (19), 17475-17482, (2003). D.M. Swank, A.F. Knowles, F. Sarsoza, J.A. Suggs, D.W. Maughan, and S.I. Bernstein, “The Myosin Converter Domain Modulates Muscle Performance,” Nature Cell Biology, 4, 312-317, (2002).
D.M. Swank, M.L. Bartoo, A.F. Knowles, C. Iliffe, S.I. Bernstein, J.E. Molloy, and J.C. Sparrow, “Alternative Exon-Encoded Regions of Drosophila Myosin Heavy Chain Modulate ATPase Rates and Actin Sliding Velocity,” Journal of Biological Chemistry, 276, (18), 15117-15124, (2001).
D.M. Swank, L. Wells, W.K. Kronert, G. Morrill, and S.I Bernstein, “Determining Structure/Function Relationships for Sarcomeric Myosin Heavy Chain by Genetic and Transgenic Manipulation of Drosophila,” Microscopy Research and Technique, 50, 430-442, (2000).
D.M. Swank and L.C. Rome, “The Influence of Temperature on Power Production During Swimming. I. In Vivo Length Change and Stimulation Pattern, Journal of Experimental Biology, 203, (2), 321-331, (2000).
D.M. Swank, G. Zhang, and L.C. Rome, “Contraction Kinetics of Red Muscle in Scup: Mechanism for Variation in Relaxation Rate Along the Length of the Fish,” Journal of Experimental Biology, 200, 1297-1307, (1997).
L.C. Rome, D.M. Swank, and D. Corda, “How Fish Power Swimming,” Science, 261, 340-343, (1993).
Contact Information:
Douglas Swank
(518) 276-4174
swankd@rpi.edu
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