ArticleMolecular biology of the cell2008
Myosin transducer mutations differentially affect motor function, myofibril structure, and the performance of skeletal and cardiac muscles.
Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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61 citing papers in PubMed, 88 citations in OpenAlex.
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- Myosin dilated cardiomyopathy mutation S532P disrupts actomyosin interactions, leading to altered muscle kinetics, reduced locomotion, and cardiac dilation inMolecular biology of the cell · 2021Article
- Modulation of post-powerstroke dynamics in myosin II by 2'-deoxy-ADP.Archives of biochemistry and biophysics · 2021Article
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- Prolonged Exposure to Microgravity Reduces Cardiac Contractility and Initiates Remodeling in Drosophila.Cell reports · 2020Article
- Overexpression ofJournal of cardiovascular development and disease · 2020Article
- A role for actin flexibility in thin filament-mediated contractile regulation and myopathy.Nature communications · 2020Article
- As time flies by: Investigating cardiac aging in the short-lived Drosophila model.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- Reductions in ATPase activity, actin sliding velocity, and myofibril stability yield muscle dysfunction in Drosophila models of myosin-based Freeman-Sheldon syndrome.Molecular biology of the cell · 2019Article
- Effects of Modest Hypoxia and Exercise on Cardiac Function, Sleep-Activity, Negative Geotaxis Behavior of Aged FemaleFrontiers in physiology · 2019Article
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- Fropofol decreases force development in cardiac muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Distinct domains in the matricellular protein Lonely heart are crucial for cardiac extracellular matrix formation and heart function inThe Journal of biological chemistry · 2018Article
- Extracellular matrix downregulation in the Drosophila heart preserves contractile function and improves lifespan.Matrix biology : journal of the International Society for Matrix Biology · 2017Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Striated muscle myosin is a multidomain ATP-dependent molecular motor. Alterations to various domains affect the chemomechanical properties of the motor, and they are associated with skeletal and cardiac myopathies. The myosin transducer domain is located near the nucleotide-binding site. Here, we helped define the role of the transducer by using an integrative approach to study how Drosophila melanogaster transducer mutations D45 and Mhc(5) affect myosin function and skeletal and cardiac muscle structure and performance. We found D45 (A261T) myosin has depressed ATPase activity and in vitro actin motility, whereas Mhc(5) (G200D) myosin has these properties enhanced. Depressed D45 myosin activity protects against age-associated dysfunction in metabolically demanding skeletal muscles. In contrast, enhanced Mhc(5) myosin function allows normal skeletal myofibril assembly, but it induces degradation of the myofibrillar apparatus, probably as a result of contractile disinhibition. Analysis of beating hearts demonstrates depressed motor function evokes a dilatory response, similar to that seen with vertebrate dilated cardiomyopathy myosin mutations, and it disrupts contractile rhythmicity. Enhanced myosin performance generates a phenotype apparently analogous to that of human restrictive cardiomyopathy, possibly indicating myosin-based origins for the disease. The D45 and Mhc(5) mutations illustrate the transducer's role in influencing the chemomechanical properties of myosin and produce unique pathologies in distinct muscles. Our data suggest Drosophila is a valuable system for identifying and modeling mutations analogous to those associated with specific human muscle disorders.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.