Through mechanical forces, biological cells remodel the surrounding collagen network, generating striking deformation patterns. Tethers—tracts of high densification and fibre alignment—form between cells, thinner bands emanate from cell clusters. While tethers facilitate cell migration and communication, how they form is unclear. Combining modelling, simulation and experiment, we show that tether formation is a densification phase transition of the extracellular matrix, caused by buckling instability of network fibres under cell-induced compression, featuring unexpected similarities with martensitic microstructures. Multiscale averaging yields a two-phase, bistable continuum energy landscape for fibrous collagen, with a densified/aligned second phase. Simulations predict strain discontinuities between the undensified and densified phase, which localizes within tethers as experimentally observed. In our experiments, active particles induce similar localized patterns as cells. This shows how cells exploit an instability to mechanically remodel the extracellular matrix simply by contracting, thereby facilitating mechanosensing, invasion and metastasis.

通过机械力，生物细胞重塑周围的胶原网络，产生惊人的变形模式。系绳——高密度和纤维排列的束——在细胞之间形成，更细的带从细胞簇中散发出来。虽然系绳有助于细胞迁移和交流，但它们是如何形成的尚不清楚。结合建模、模拟和实验，我们表明系链形成是细胞外基质的致密化相变，由细胞诱导压缩下网络纤维的屈曲不稳定性引起，与马氏体微观结构具有意想不到的相似性。多尺度平均产生纤维胶原的双相、双稳态连续能量景观，具有致密/对齐的第二相。模拟预测未致密相和致密相之间的应变不连续性，如实验观察到的那样，它定位在系绳内。在我们的实验中，活性粒子会诱导与细胞相似的局部模式。这显示了细胞如何利用不稳定性来简单地通过收缩来机械地重塑细胞外基质，从而促进机械传感、侵袭和转移。