Link to bioRxiv paper:
http://biorxiv.org/cgi/content/short/2023.04.13.536664v1?rss=1

Authors: Yi, X., Chen, P., Kang, C., Li, D., Yang, Y., Cai, H., Li, B., Wu, C.

Abstract:
Cell migration towards stiff substrates has been coined as durotaxis and implicated in development, wound healing and cancer, where complex interplays between immune and non-immune cells are present. Compared to the emerging mechanisms underlying the strongly adhesive mesenchymal durotaxis, little is known about whether immune cells - migrating in amoeboid mode - could follow mechanical cues. Here we develop an imaging-based confined migration device that provides stiffness gradient for cell migration. By tracking live cell trajectory and analyzing the directionality T cells and neutrophils, we observe that amoeboid cells can durotax. We further delineate the underlying mechanism to involve non-muscle myosin IIA (NMIIA) polarization towards the soft-matrix-side but may not require differential actin flow up- or down-stiffness gradient. Using the protista Dictyostelium, we further demonstrate the evolutionary conservation of amoeboid durotaxis. Finally, these experimental phenomena are theoretically captured by an active gel model capable of mechanosensing. Collectively, these results may shed new lights on immune surveillance and recently identified confined migration of cancer cells, within the tumor microenvironment or the inflamed fibrotic tissues.

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