Journal
PROCEEDINGS OF THE JAPAN ACADEMY SERIES B-PHYSICAL AND BIOLOGICAL SCIENCES
Volume 91, Issue 7, Pages 321-350Publisher
JAPAN ACAD
DOI: 10.2183/pjab.91.321
Keywords
striated muscle; calcium-regulation; actin; tropomyosin; troponin; cardiomyopathy
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Funding
- Ministry of Education, Science, Culture and Sports, Science and Technology of Japan
- Institute of Physical Chemical Research (RIKEN)
- HFSP (Human Frontier Science Foundation)
- Mitsubishi Foundation
- Toray Science Foundation
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The author reviewed the research that led to establish the structural basis for the mechanism of the calcium-regulation of the contraction of striated muscles. The target of calcium ions is troponin on the thin filaments, of which the main component is the double-stranded helix of actin. A model of thin filament was generated by adding tropomyosin and troponin. During the process to provide the structural evidence for the model, the troponin arm was found to protrude from the calcium-depleted troponin and binds to the carboxyl-terminal region of actin. As a result, the carboxyl-terminal region of tropomyosin shifts and covers the myosin-binding sites of actin to block the binding of myosin. At higher calcium concentrations, the troponin arm changes its partner from actin to the main body of calcium-loaded troponin. Then, tropomyosin shifts back to the position near the grooves of actin double helix, and the myosin-binding sites of actin becomes available to myosin resulting in force generation through actin-myosin interactions.
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