Historical Aspects -- Biological Actions of Calcium -- Professor Ebashi's Journey Toward the Discovery of Troponin: A Personal Recollection -- Highlights of the History of Calcium Regulation of Striated Muscle -- Regulation by Troponin and Tropomyosin -- Troponin: Structure, Function and Dysfunction -- From the Crystal Structure of Troponin to the Mechanism of Calcium Regulation of Muscle Contraction -- Ca Ion and the Troponin Switch -- Disposition and Dynamics: Interdomain Orientations in Troponin -- Structural Basis for Calcium-Regulated Relaxation of Striated Muscles at Interaction Sites of Troponin with Actin and Tropomyosin -- Tropomyosin: Regulator of Actin Filaments -- Tropomyosin and Troponin Cooperativity on the Thin Filament -- Conformational Changes in Reconstituted Skeletal Muscle Thin Filaments Observed by Fluorescence Spectroscopy -- Calcium Structural Transition of Troponin in the Complexes, on the Thin Filament, and in Muscle Fibres, as Studied By Site-Directed Spin-Labelling EPR -- Crystal Structures of Tropomyosin: Flexible Coiled-Coil -- C. Elegans Model for Studying Tropomyosin and Troponin Regulations of Muscle Contraction and Animal Behavior -- Structural and Functional Analysis of Troponins from Scallop Striated and Human Cardiac Muscles -- Regulation in Cardiac Muscle and Disorders -- Cooperativity in the Regulation of Force and the Kinetics of Force Development in Heart and Skeletal Muscles -- Heart Failure, Ischemia/Reperfusion Injury and Cardiac Troponin -- Troponin Mutations in Cardiomyopathies -- Molecular Pathogenic Mechanisms of Cardiomyopathies Caused by Mutations in Cardiac Troponin T -- Cardiac Troponin Levels as a Preferable Biomarker of Myocardial Cell Degradation -- Regulation by Myosin -- Regulation by Myosin: How Calcium Regulates Some Myosins, Past and Present -- Calcium Inhibition of Physarum Myosin as Examined by the Recombinant Heavy Mero-Myosin -- Excitation-Contraction Coupling and Disorder -- Calcium-Induced Release of Calcium From the Sarcoplasmic Reticulum -- Dysregulation of the Gain of CICR Through Ryanodine Receptor1 (RyR1): The Putative Mechanism Underlying Malignant Hyperthermia -- Ion Pumping by Calcium ATPase of Sarcoplasmic Reticulum -- Regulation of Cell Functions by Ca2+ Oscillation -- Molecular Mechanisms of Muscle Contraction -- Evidence About the Structural Behaviour of Myosin Crossbridges During Muscle Contraction -- Structural Alterations of Thin Actin Filaments in Muscle Contraction by Synchrotron X-ray Fiber Diffraction -- Regulation of Muscle Contraction by Ca2+ and ADP: Focusing on the0 Auto-Oscillation (SPOC) -- Muscle Contraction Mechanism Based on Actin Filament Rotation -- On the Walking Mechanism of Linear Molecular Motors -- Modeling of the F-Actin Structure. The discovery of troponin by Professor Setsuro Ebashi opened a new era for research into the regulation of striated muscle contraction. This volume is the proceedings of the s- posium held at Okazaki, Japan, in 2005 celebrating the 40th anniversary of that discovery. Professor Ebashi started his work on muscle contraction when he was a young researcher, immediately after World War II, having been inspired by the book Chemistry of Muscular Contraction by Albert Szent-Györgyi. He was fascinated by the dynamic features of the contractile processes performed by the two contractile proteins, myosin and actin, in the presence of ATP. However, he wondered about the mechanism by which muscle relaxes after contraction. He proceeded with biochemical studies of muscle rel- ation and found in 1952 that a factor present in the supernatant of the suspension of minced frog skeletal muscle caused relaxation of glycerinated muscle ?bers. Based on this ?nding and succeeding work, he came to the conclusion that the relaxation of c- tracted muscle was caused by the uptake of calcium ions from the cytosol into the relaxing factor (sarcoplasmic reticulum). His work greatly contributed to elucidating the entire processes of excitation-contraction coupling, particularly the role of calcium ions in tr- gering the contractile response of myo?brils. Then he found that superprecipitation of actomyosin, i. e. , an in vitro contraction model, became sensitive to calcium ion concentration in the presence of a protein factor other than myosin and actin.