ArticleBiophysical journal2011
Regulatory light chain phosphorylation and N-terminal extension increase cross-bridge binding and power output in Drosophila at in vivo myofilament lattice spacing.
Article in Biophysical journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Persistent viral infections impact key biological traits in Drosophila melanogaster.PLoS biology · 2025Article
- Small Angle X-ray Diffraction as a Tool for Structural Characterization of Muscle Disease.International journal of molecular sciences · 2022Review
- X-ray Crystallographic and Molecular Dynamic Analyses of Drosophila melanogaster Embryonic Muscle Myosin Define Domains Responsible for Isoform-Specific Properties.Journal of molecular biology · 2020Article
- Evolution of Flight Muscle Contractility and Energetic Efficiency.Frontiers in physiology · 2020Review
- Insights into Actin-Myosin Interactions within Muscle from 3D Electron Microscopy.International journal of molecular sciences · 2019Review
- Flightin maintains myofilament lattice organization required for optimal flight power and courtship song quality inProceedings. Biological sciences · 2017Article
- Phosphorylation of the regulatory light chain of myosin in striated muscle: methodological perspectives.European biophysics journal : EBJ · 2016Review
- Structure of myosin filaments from relaxedScience advances · 2016Article
- In vitro and in vivo single myosin step-sizes in striated muscle.Journal of muscle research and cell motility · 2015Article
- Constitutive phosphorylation of cardiac myosin regulatory light chain prevents development of hypertrophic cardiomyopathy in mice.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Myosin light chains: Teaching old dogs new tricks.Bioarchitecture · 2014Review
- Mutations of the Drosophila myosin regulatory light chain affect courtship song and reduce reproductive success.PloS one · 2014Article
- X-ray diffraction from flight muscle with a headless myosin mutation: implications for interpreting reflection patterns.Frontiers in physiology · 2014Article
- Myosin phosphorylation and force potentiation in skeletal muscle: evidence from animal models.Journal of muscle research and cell motility · 2013Review
- Age-related slowing of myosin actin cross-bridge kinetics is sex specific and predicts decrements in whole skeletal muscle performance in humans.Journal of applied physiology (Bethesda, Md. : 1985) · 2013Article
- Thick-to-thin filament surface distance modulates cross-bridge kinetics in Drosophila flight muscle.Biophysical journal · 2012Article
- Structure, interactions and function of the N-terminus of cardiac myosin binding protein C (MyBP-C): who does what, with what, and to whom?Journal of muscle research and cell motility · 2012Review
- Structural and functional aspects of the myosin essential light chain in cardiac muscle contraction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- Regulating the contraction of insect flight muscle.Journal of muscle research and cell motility · 2011Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The N-terminal extension and phosphorylation of the myosin regulatory light chain (RLC) independently improve Drosophila melanogaster flight performance. Here we examine the functional and structural role of the RLC in chemically skinned fibers at various thick and thin filament lattice spacings from four transgenic Drosophila lines: rescued null or control (Dmlc2(+)), truncated N-terminal extension (Dmlc2(Δ2-46)), disrupted myosin light chain kinase phosphorylation sites (Dmlc2(S66A,S67A)), and dual mutant (Dmlc2(Δ2-46; S66A,S67A)). The N-terminal extension truncation and phosphorylation sites disruption mutations decreased oscillatory power output and the frequency of maximum power output in maximally Ca(2+)-activated fibers compressed to near in vivo inter-thick filament spacing, with the phosphorylation sites disruption mutation having a larger affect. The diminished power output parameters with the N-terminal extension truncation and phosphorylation sites disruption mutations were due to the reduction of the number of strongly-bound cross-bridges and rate of myosin force production, with the larger parameter reductions in the phosphorylation sites disruption mutation additionally related to reduced myosin attachment time. The phosphorylation and N-terminal extension-dependent boost in cross-bridge kinetics corroborates previous structural data, which indicate these RLC attributes play a complementary role in moving and orienting myosin heads toward actin target sites, thereby increasing fiber and whole fly power generation.
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Registered trials
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.