ArticleMolecular biology of the cell2017
Local Arp2/3-dependent actin assembly modulates applied traction force during apCAM adhesion site maturation.
Article in Molecular biology of the cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 9 citations in OpenAlex.
- Growth cone macropinocytosis of neurotrophin receptor and neuritogenesis are regulated by neuron navigator 1.Molecular biology of the cell · 2022Article
- The Arp2/3 complex is crucial for colonisation of the mouse skin by melanoblasts.Development (Cambridge, England) · 2020Article
- An Integrated Cytoskeletal Model of Neurite Outgrowth.Frontiers in cellular neuroscience · 2018Review
- Actin-based growth cone motility and guidance.Molecular and cellular neurosciences · 2017Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Homophilic binding of immunoglobulin superfamily molecules such as the Aplysia cell adhesion molecule (apCAM) leads to actin filament assembly near nascent adhesion sites. Such actin assembly can generate significant localized forces that have not been characterized in the larger context of axon growth and guidance. We used apCAM-coated bead substrates applied to the surface of neuronal growth cones to characterize the development of forces evoked by varying stiffness of mechanical restraint. Unrestrained bead propulsion matched or exceeded rates of retrograde network flow and was dependent on Arp2/3 complex activity. Analysis of growth cone forces applied to beads at low stiffness of restraint revealed switching between two states: frictional coupling to retrograde flow and Arp2/3-dependent propulsion. Stiff mechanical restraint led to formation of an extensive actin cup matching the geometric profile of the bead target and forward growth cone translocation; pharmacological inhibition of the Arp2/3 complex or Rac attenuated F-actin assembly near bead binding sites, decreased the efficacy of growth responses, and blocked accumulation of signaling molecules associated with nascent adhesions. These studies introduce a new model for regulation of traction force in which local actin assembly forces buffer nascent adhesion sites from the mechanical effects of retrograde flow.
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Registered trials
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