About the event
Dr. Daniel Fitzsimons, Assistant Professor, Department of Animal, Veterinary & Food Sciences, University of Idaho
Dr. Daniel Fitzsimons received both his B.S. degree in Biological Sciences and his Ph.D. in Physiology and Biophysics, from the University of California, Irvine. After receiving his Ph.D., Dr. Fitzsimons joined the University of Wisconsin-Madison, where he served as a Researcher and Associate Scientist in the Department of Physiology until 2012. He then joined the Department of Cell and Regenerative Biology, at the University of Wisconsin School of Medicine, where he worked until joining the University of Idaho in 2020. Dr. Fitzsimons’s laboratory studies the contractile processes in heart and alterations in contraction in diseases such as cardiomyopathy. A primary focus of his research is the set of molecular mechanisms underlying the cooperative modulation of contraction and relaxation in the human heart.
Ca2+ binding to troponin C and myosin cross-bridge binding to actin act in a synergistic, cooperative manner to modulate myocardial contraction and relaxation. The responsiveness of the myocardial thin filament to activating effects of Ca2+ and myosin cross-bridge binding (i.e., the cooperative phenotype) have been well-characterized in the myocardium of small mammals (i.e., rodents). Given the ten-fold difference in resting heart rates and twitch kinetics between small and large mammals, it is likely that the cooperative phenotype is a species-dependent property of mammalian myocardium instances. Such a mechanism suggests a molecular basis for beat-to-beat synchronization of ventricular contractility and circulatory demand.