Mechanochemical interactions dictate obstacle-induced cell turning by breaking symmetry in actin dynamics
- 1School of Science, Harbin Institute of Technology
- 2Department of Pulmonary and Critical Care Medicine, Shenzhen Key Laboratory of Respiratory Diseases, Shenzhen Clinical Research Center for Respiratory Disease, Shenzhen Institute of Respiratory Diseases, Shenzhen People’s Hospital (The First Affiliated Hospital, Southern University of Science and Technology, The Second Clinical Medical College, Jinan University)
Abstract
Cell turning enables cells to navigate complex tissue environments, yet its mechanistic basis remains unclear. Here we develop a theoretical framework showing how the obstacle-induced turning is initiated, amplified, and regulated. Turning arises from a self-organized asymmetry between actin polymerization and retrograde flow at the leading edge, which is maximized at an optimal substrate stiffness (~0.1–1 pN/nm). In this range, adhesion engagement most effectively suppresses retrograde flow and redirects protrusion, whereas obstacle stiffness has negligible influence, demonstrating that substrate–clutch mechanics dominate the actin response to compression. We further show that elevated diffusion selectively enhances polymerization at the free edge without altering dynamics at the constrained edge. Meanwhile, chemotactic signaling spatially redistributes Arp2/3 and myosin II to strengthen protrusion away from the obstacle while increasing contractility near it. This dual remodeling increases turning rates and shifts the optimal stiffness for maximal reorientation. Together, our findings reveal cell turning as an active, tunable mechanochemical process driven by breaking symmetry of actin dynamics.
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BibTeX
@article{shao2026mechanochemical,
title = {{Mechanochemical interactions dictate obstacle-induced cell turning by breaking symmetry in actin dynamics}},
author = {Yaobi Shao and Yuanyuan Liu and Chao Fang},
journal = {Communications Physics},
year = {2026},
month = jul,
doi = {10.1038/s42005-026-02744-y},
url = {https://doi.org/10.1038/s42005-026-02744-y},
note = {CC BY},
}
RIS
TY - JOUR
TI - Mechanochemical interactions dictate obstacle-induced cell turning by breaking symmetry in actin dynamics
AU - Yaobi Shao
AU - Yuanyuan Liu
AU - Chao Fang
PY - 2026
DA - 2026/07/01
JO - Communications Physics
DO - 10.1038/s42005-026-02744-y
UR - https://doi.org/10.1038/s42005-026-02744-y
AB - Cell turning enables cells to navigate complex tissue environments, yet its mechanistic basis remains unclear. Here we develop a theoretical framework showing how the obstacle-induced turning is initiated, amplified, and regulated. Turning arises from a self-organized asymmetry between actin polymerization and retrograde flow at the leading edge, which is maximized at an optimal substrate stiffness (~0.1–1 pN/nm). In this range, adhesion engagement most effectively suppresses retrograde flow and redirects protrusion, whereas obstacle stiffness has negligible influence, demonstrating that substrate–clutch mechanics dominate the actin response to compression. We further show that elevated diffusion selectively enhances polymerization at the free edge without altering dynamics at the constrained edge. Meanwhile, chemotactic signaling spatially redistributes Arp2/3 and myosin II to strengthen protrusion away from the obstacle while increasing contractility near it. This dual remodeling increases turning rates and shifts the optimal stiffness for maximal reorientation. Together, our findings reveal cell turning as an active, tunable mechanochemical process driven by breaking symmetry of actin dynamics.
SN - 2399-3650
ER -