Thick and thin filament effectors of cardiac myofibril contraction detected in a troponin c-based high-throughput fluorescence lifetime assay

Abstract

Cardiac muscle contraction is initiated by Ca2+-induced structural changes of the thin filaments to permit cross-bridge formation. Ca2+ binding to cardiac troponin C (TnC) on actin permits myosin binding and ATP binding to myosin allows for cross-bridge cycling during contraction. Site-directed spectroscopic probes attached to TnC at position T53C have been useful to determine structure-function relationships and Ca2+ binding kinetics in thin filaments and myofibrils by monitoring fluorescence intensity.