Ca2+ and Myosin Cycle States Work as Allosteric Effectors of Troponin Activation

In cardiac muscle, troponin (Tn) and tropomyosin (Tm) inhibit actin and myosin interactions through the steric blocking of myosin binding to F-actin. Ca2+ binding to TnC modulates this inhibition. Thin filaments become activated upon Ca2+ binding, which enables strong binding of myosin with concomitant release of ATP hydrolysis products and level arm swinging responsible for force generation. Despite this level of description, the current cross-bridge cycle model does not fully define the structural events that take place within Tn during combinatorial myosin and Ca2+ interventions.

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