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Cells in monolayers, considered active nematics, unexpectedly migrate toward all +1 topological defects. This challenges existing theories and reveals new nonlinear forces governing cell behavior.

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Area of Science:

  • Cell biology
  • Active matter physics
  • Soft condensed matter

Background:

  • Confluent monolayers of elongated cells exhibit active nematic behavior with topological defects.
  • Existing models predict cell accumulation at +1 defects in extensile systems and escape from -1 defects.
  • Collective cell dynamics around integer topological defects are not fully understood.

Purpose of the Study:

  • To investigate the collective dynamics of neural progenitor cell monolayers around diverse +1 topological defects.
  • To challenge conventional theories on cell behavior at topological defects.
  • To identify underlying mechanisms driving cell migration toward defect cores.

Main Methods:

  • Induction of +1 topological defects (asters, spirals, targets) in cell monolayers using microfabricated patterns.
  • Experimental observation of cell migration patterns.
  • Development and application of a continuum theory derived from a cell-level model.

Main Results:

  • Cells consistently migrated toward the cores of all induced +1 topological defects, regardless of defect type.
  • This behavior contradicts predictions of conventional extensile/contractile models for spiral and target defects.
  • Nonlinear active forces, previously overlooked, were identified as driving the accumulation toward defect cores.

Conclusions:

  • A unified framework explaining cell accumulation at various +1 defects was established.
  • +1 topological defects serve as effective probes for uncovering nonlinear features in active nematics.
  • The study provides a methodology for characterizing and classifying cell monolayers based on their nematic behavior.