ArticleJournal of molecular biology2009
Structural basis for the activation of muscle contraction by troponin and tropomyosin.
Article in Journal of molecular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed.
- The precise nutritional roles of calcium and phosphorus and the synergistic effects and mechanisms in chicken.Poultry science · 2026Review
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- Transcriptomic analysis demonstrates moderators of muscle quality are altered in age-related sarcopenic obesity.BMC genomics · 2025Article
- Diacylglycerol metabolism drives host-pathogen responses during enteric infection inbioRxiv : the preprint server for biology · 2025Article
- Hypocalcaemic cardiomyopathy presenting as heart failure exacerbation due to untreated primary hypoparathyroidism.ESC heart failure · 2025Article
- The unique biology of catch muscles: insights into structure, function, and robotics innovations.Frontiers in bioengineering and biotechnology · 2025Review
- Beet curly top virus affects vector biology: the first transcriptome analysis of the beet leafhopper.The Journal of general virology · 2024Article
- Cooperativity of myosin II motors in the non-regulated and regulated thin filaments investigated with high-speed AFM.The Journal of general physiology · 2023Article
- Motor dysfunction iniScience · 2022Article
- RNAi for Western Corn Rootworm Management: Lessons Learned, Challenges, and Future Directions.Insects · 2022Review
- Single-molecule imaging reveals the concerted release of myosin from regulated thin filaments.eLife · 2021Article
- Loss of crossbridge inhibition drives pathological cardiac hypertrophy in patients harboring the TPM1 E192K mutation.The Journal of general physiology · 2021Article
- The actin 'A-triad's' role in contractile regulation in health and disease.The Journal of physiology · 2020Review
- Cytoskeleton-a crucial key in host cell for coronavirus infection.Journal of molecular cell biology · 2020Review
- A Stochastic Multiscale Model of Cardiac Thin Filament Activation Using Brownian-Langevin Dynamics.Biophysical journal · 2019Article
- New Insights in Cardiac Calcium Handling and Excitation-Contraction Coupling.Advances in experimental medicine and biology · 2018Review
- Tropomyosin Must Interact Weakly with Actin to Effectively Regulate Thin Filament Function.Biophysical journal · 2017Article
- Distortion of the Actin A-Triad Results in Contractile Disinhibition and Cardiomyopathy.Cell reports · 2017Article
- Role of cardiac troponin I carboxy terminal mobile domain and linker sequence in regulating cardiac contraction.Archives of biochemistry and biophysics · 2016Article
- Structural determinants of muscle thin filament cooperativity.Archives of biochemistry and biophysics · 2016Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
The molecular regulation of striated muscle contraction couples the binding and dissociation of Ca(2+) on troponin (Tn) to the movement of tropomyosin on actin filaments. In turn, this process exposes or blocks myosin binding sites on actin, thereby controlling myosin crossbridge dynamics and consequently muscle contraction. Using 3D electron microscopy, we recently provided structural evidence that a C-terminal extension of TnI is anchored on actin at low Ca(2+) and competes with tropomyosin for a common site to drive tropomyosin to the B-state location, a constrained, relaxing position on actin that inhibits myosin-crossbridge association. Here, we show that release of this constraint at high Ca(2+) allows a second segment of troponin, probably representing parts of TnT or the troponin core domain, to promote tropomyosin movement on actin to the Ca(2+)-induced C-state location. With tropomyosin stabilized in this position, myosin binding interactions can begin. Tropomyosin appears to oscillate to a higher degree between respective B- and C-state positions on troponin-free filaments than on fully regulated filaments, suggesting that tropomyosin positioning in both states is troponin-dependent. By biasing tropomyosin to either of these two positions, troponin appears to have two distinct structural functions; in relaxed muscles at low Ca(2+), troponin operates as an inhibitor, while in activated muscles at high Ca(2+), it acts as a promoter to initiate contraction.
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Registered trials
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