Integer topological defects offer a methodology to quantify and classify active cell monolayers.

Abstract

Monolayers of confluent elongated cells are frequently considered active nematics, featuring <math xmlns="http://www.w3.org/1998/Math/MathML"><mo>±</mo> <mfrac><mrow><mn>1</mn></mrow> <mrow><mn>2</mn></mrow> </mfrac> </math> topological defects. In extensile systems, where cells extend further along their long axis, they can accumulate at <math xmlns="http://www.w3.org/1998/Math/MathML"><mo>+</mo> <mfrac><mrow><mn>1</mn></mrow> <mrow><mn>2</mn></mrow> </mfrac> </math> defects and escape from <math xmlns="http://www.w3.org/1998/Math/MathML"><mo>-</mo> <mfrac><mrow><mn>1</mn></mrow> <mrow><mn>2</mn></mrow> </mfrac> </math> defects. Nevertheless, collective dynamics surrounding integer defects remain insufficiently understood. We induce diverse  + 1 topological defects (asters, spirals, and targets) within neural progenitor cell monolayers using microfabricated patterns. Remarkably, cells migrate toward the cores of all  + 1 defects, challenging existing theories and conventional extensile/contractile dichotomy, which predicts escape from highly bent spirals and targets. By combining experiments and a continuum theory derived from a cell-level model, we identify previously overlooked nonlinear active forces driving this unexpected accumulation toward defect cores, providing a unified framework to explain cell behavior across defect types. Our findings establish  + 1 defects as probes to uncover key nonlinear features of active nematics, offering a methodology to characterize and classify cell monolayers.