ArticleScientific reports2015
Differential Contributions of Nonmuscle Myosin II Isoforms and Functional Domains to Stress Fiber Mechanics.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Non-muscle myosin heavy chain IIA regulates cell morphology, stress fibre structure, and cell migration in FLO-1 oesophageal adenocarcinoma cells.Human cell · 2025Article
- Limiting pool and actin architecture controls myosin cluster sizes in adherent cells.Biophysical journal · 2024Article
- From stress fiber to focal adhesion: a role of actin crosslinkers in force transmission.Frontiers in cell and developmental biology · 2024Review
- Myosin II proteins are required for organization of calcium-induced actin networks upstream of mitochondrial division.Molecular biology of the cell · 2022Article
- Synaptopodin stress fiber and contractomere at the epithelial junction.The Journal of cell biology · 2022Article
- Articular Chondrocyte Phenotype Regulation through the Cytoskeleton and the Signaling Processes That Originate from or Converge on the Cytoskeleton: Towards a Novel Understanding of the Intersection between Actin Dynamics and Chondrogenic Function.International journal of molecular sciences · 2021Review
- Mechanobiological Implications of Cancer Progression in Space.Frontiers in cell and developmental biology · 2021Review
- Myosin II isoforms play distinct roles ineLife · 2019Article
- Mammalian nonmuscle myosin II comes in three flavors.Biochemical and biophysical research communications · 2018Review
- Myosins in Osteoclast Formation and Function.Biomolecules · 2018Review
- Actomyosin stress fiber subtypes have unique viscoelastic properties and roles in tension generation.Molecular biology of the cell · 2018Article
- Different contributions of nonmuscle myosin IIA and IIB to the organization of stress fiber subtypes in fibroblasts.Molecular biology of the cell · 2018Article
- Activation of ROCK and MLCK tunes regional stress fiber formation and mechanics via preferential myosin light chain phosphorylation.Molecular biology of the cell · 2017Article
- An excitable Rho GTPase signaling network generates dynamic subcellular contraction patterns.The Journal of cell biology · 2017Article
- Geometry and network connectivity govern the mechanics of stress fibers.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Local pulsatile contractions are an intrinsic property of the myosin 2A motor in the cortical cytoskeleton of adherent cells.Molecular biology of the cell · 2017Article
- Microsurgery-aided in-situ force probing reveals extensibility and viscoelastic properties of individual stress fibers.Scientific reports · 2016Article
- Actomyosin stress fiber mechanosensing in 2D and 3D.F1000Research · 2016Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
While is widely acknowledged that nonmuscle myosin II (NMMII) enables stress fibers (SFs) to generate traction forces against the extracellular matrix, little is known about how specific NMMII isoforms and functional domains contribute to SF mechanics. Here we combine biophotonic and genetic approaches to address these open questions. First, we suppress the NMMII isoforms MIIA and MIIB and apply femtosecond laser nanosurgery to ablate and investigate the viscoelastic retraction of individual SFs. SF retraction dynamics associated with MIIA and MIIB suppression qualitatively phenocopy our earlier measurements in the setting of Rho kinase (ROCK) and myosin light chain kinase (MLCK) inhibition, respectively. Furthermore, fluorescence imaging and photobleaching recovery reveal that MIIA and MIIB are enriched in and more stably localize to ROCK- and MLCK-controlled central and peripheral SFs, respectively. Additional domain-mapping studies surprisingly reveal that deletion of the head domain speeds SF retraction, which we ascribe to reduced drag from actomyosin crosslinking and frictional losses. We propose a model in which ROCK/MIIA and MLCK/MIIB functionally regulate common pools of SFs, with MIIA crosslinking and motor functions jointly contributing to SF retraction dynamics and cellular traction forces.
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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.