ArticleProceedings of the National Academy of Sciences of the United States of America2019
Torsional stress generated by ADF/cofilin on cross-linked actin filaments boosts their severing.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
59 citing papers in PubMed, 103 citations in OpenAlex.
- Dosage-sensitive regulation of Cofilin-1 and LIMK signaling controls myoblast differentiation and fusion.Cellular and molecular life sciences : CMLS · 2026Article
- Myosin II-independent contraction of actin filaments in membrane nanotubes.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Fast Actin Disassembly and Fimbrin Mechanosensitivity Support Rapid Turnover in a Model of Clathrin-Mediated Endocytosis.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Myosin 2 - A general contractor for the cytoskeleton.Current opinion in cell biology · 2025Review
- Reconstituted systems for studying the architecture and dynamics of actin networks.The Biochemical journal · 2025Review
- Histidine 73 methylation coordinates β-actin plasticity in response to key environmental factors.Nature communications · 2025Article
- Multiple Mechanisms to Regulate Actin Functions: "Fundamental" Versus Lineage-Specific Mechanisms and Hierarchical Relationships.Biomolecules · 2025Review
- Comparing simulations of actin filament compression reveals tradeoff between computational cost and capturing supertwist.microPublication biology · 2025Article
- Cracked actin filaments as mechanosensitive receptors.Biophysical journal · 2024Article
- Principles and regulation of mechanosensing.Journal of cell science · 2024Review
- Single-pericyte nanomechanics measured by contraction cytometry.APL bioengineering · 2024Article
- Myosin forces elicit an F-actin structural landscape that mediates mechanosensitive protein recognition.bioRxiv : the preprint server for biology · 2024Article
- Myosin-induced F-actin fragmentation facilitates contraction of actin networks.Cytoskeleton (Hoboken, N.J.) · 2024Article
- Fascin-induced bundling protects actin filaments from disassembly by cofilin.The Journal of cell biology · 2024Article
- Two Septin complexes mediate actin dynamics during cell wound repair.Cell reports · 2024Article
- Cytokinetic abscission requires actin-dependent microtubule severing.Nature communications · 2024Article
- Cofilin-mediated actin filament network flexibility facilitates 2D to 3D actomyosin shape change.European journal of cell biology · 2024Article
- The stabilization of Arp2/3 complex generated actin filaments.Biochemical Society transactions · 2024Review
- Regeneration of actin filament branches from the same Arp2/3 complex.Science advances · 2024Article
- Mechanisms of actin disassembly and turnover.The Journal of cell biology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proteins of the actin depolymerizing factor (ADF)/cofilin family are the central regulators of actin filament disassembly. A key function of ADF/cofilin is to sever actin filaments. However, how it does so in a physiological context, where filaments are interconnected and under mechanical stress, remains unclear. Here, we monitor and quantify the action of ADF/cofilin in different mechanical situations by using single-molecule, single-filament, and filament network techniques, coupled to microfluidics. We find that local curvature favors severing, while tension surprisingly has no effect on cofilin binding and weakly enhances severing. Remarkably, we observe that filament segments that are held between two anchoring points, thereby constraining their twist, experience a mechanical torque upon cofilin binding. We find that this ADF/cofilin-induced torque does not hinder ADF/cofilin binding, but dramatically enhances severing. A simple model, which faithfully recapitulates our experimental observations, indicates that the ADF/cofilin-induced torque increases the severing rate constant 100-fold. A consequence of this mechanism, which we verify experimentally, is that cross-linked filament networks are severed by cofilin far more efficiently than nonconnected filaments. We propose that this mechanochemical mechanism is critical to boost ADF/cofilin's ability to sever highly connected filament networks in cells.
Indexed as
Identifiers
What OpenQuestion holds
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.