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<p>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.</p>

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Mechanochemical interactions dictate obstacle-induced cell turning by breaking symmetry in actin dynamics

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月10日

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  • Yaobi Shao,
  • Yuanyuan Liu,
  • Chao Fang

摘要

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.