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<p>Active solids using energy influx to generate non-equilibrium forces undergo spontaneous mechanical failure, but how topological defects concentrate internal stresses and control breakage in active materials is unknown. Here we assemble a reconstituted two-dimensional actomyosin network that lacks fluidity but exhibits nematic order and network elasticity. Surprisingly, we found that interacting multidefect configurations, especially defect quadrupoles with two +1/2 and two −1/2 defects, play a crucial role. Combining experimental data with an active solid fracture model, we demonstrate that a head quadrupole with mutually facing +1/2 defects can trigger crack opening and material tearing. Meanwhile, tail quadrupoles with mutually opposing +1/2 defects drive transient filament clustering and condenses into asters. We establish a deep learning model to predict the eventual aster formation from the initial topological structures. Our work uncovers a defect-mediated mechanism for spontaneous failure in active solids and provides topological design principles for controlling targeted damage in soft and living systems across scales.</p>

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Topological control of spontaneous failure in active nematic solids

  • 期刊论文

  • 发表日期：

    2026年2月25日

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  • Sheng Chen,
  • Matthew Ricci,
  • A. Pasha Tabatabai,
  • Zachary Gao Sun,
  • Sven Witthaus,
  • Suraj Shankar,
  • Mor Nitzan,
  • Michael P. Murrell

摘要

Active solids using energy influx to generate non-equilibrium forces undergo spontaneous mechanical failure, but how topological defects concentrate internal stresses and control breakage in active materials is unknown. Here we assemble a reconstituted two-dimensional actomyosin network that lacks fluidity but exhibits nematic order and network elasticity. Surprisingly, we found that interacting multidefect configurations, especially defect quadrupoles with two +1/2 and two −1/2 defects, play a crucial role. Combining experimental data with an active solid fracture model, we demonstrate that a head quadrupole with mutually facing +1/2 defects can trigger crack opening and material tearing. Meanwhile, tail quadrupoles with mutually opposing +1/2 defects drive transient filament clustering and condenses into asters. We establish a deep learning model to predict the eventual aster formation from the initial topological structures. Our work uncovers a defect-mediated mechanism for spontaneous failure in active solids and provides topological design principles for controlling targeted damage in soft and living systems across scales.