[Paper Review] Motility initiation in active gels

Pierre Recho, Thibaut Putelat+1 more|arXiv (Cornell University)|Jan 28, 2015

Micro and Nano Robotics100 references3 citations

TL;DR

This paper proposes that increased contractility in active gels—modeled as a proxy for crawling cells—drives both symmetry breaking and initial motility, with excessive contraction causing transient stalling and re-symmetrization. The theory reproduces keratocyte motility initiation patterns and pre-divisional behaviors, linking contractility dynamics to cellular polarity and movement transitions.

ABSTRACT

Motility initiation in crawling cells requires a symmetry breaking mechanism which transforms a symmetric state into a polarized state. Experiments on keratocytes suggest that polarization is triggered by increased contractility of motor proteins. In this paper we argue that contraction can be responsible not only for the symmetry breaking transition but also for the incipient translocation of the segment of an active gel mimicking the crawling cell. Our model suggests that when the contractility increases sufficiently far beyond the motility initiation threshold, the cell can stop and re-symmetrizes. The proposed theory reproduces the motility initiation pattern in fish keratocytes and the behavior of keratocytes prior to cell division.

Motivation & Objective

• To understand the mechanism by which active gels transition from symmetric to polarized states during cell motility.
• To investigate how contractility in motor proteins triggers both symmetry breaking and incipient translocation in a crawling cell model.
• To explore the conditions under which excessive contractility leads to transient stalling and re-symmetrization in the motility cycle.
• To reproduce experimentally observed motility patterns in fish keratocytes and their behavior prior to cell division using a minimal active gel model.

Proposed method

• Modeling a two-dimensional active gel with tunable contractility to simulate the mechanical behavior of a crawling cell.
• Introducing a contractility parameter that exceeds a critical threshold to induce symmetry breaking and initiate motility.
• Using continuum mechanics and active matter theory to describe the feedback between contractility and gel deformation.
• Analyzing the system's response beyond the initiation threshold to identify conditions leading to transient stalling and re-symmetrization.
• Comparing model predictions with experimental data on keratocyte motility and pre-divisional dynamics.

Experimental results

Research questions

• RQ1 How does increased contractility in an active gel lead to symmetry breaking and the onset of motility?
• RQ2 What happens to the system when contractility exceeds the motility initiation threshold?
• RQ3 Can the model reproduce the characteristic motility initiation pattern observed in fish keratocytes?
• RQ4 Does the model capture the transient re-symmetrization behavior seen in keratocytes prior to cell division?

Key findings

• Contractility increase beyond the motility initiation threshold leads to transient stalling and re-symmetrization of the active gel.
• The model successfully reproduces the experimentally observed motility initiation pattern in fish keratocytes.
• The system exhibits a non-monotonic response to contractility, with motility emerging only within a specific range of contractile forces.
• The model captures the pre-divisional behavior of keratocytes, including polarity loss and reorganization, through contractility dynamics.