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Thibaut Putelat

Publications and source records attributed to Thibaut Putelat.

3 recordsLinked to original sources

Colliding cells: when active segments behave as active particles

Quantifying the outcomes of cells collisions is a crucial step in building the foundations of a kinetic theory of living matter. Here, we develop a mechanical theory of such collisions by first representing individual cells as extended objects with internal activity and then reducing this description to a model of size-less active particles characterized by their position and polarity. We show that, in the presence of an applied force, a cell can either be dragged along or self-propel against the force, depending on the polarity of the cell. The co-existence of these regimes offers a self-consistent mechanical explanation for cell re-polarization upon contact. We rationalize the experimentally observed collision scenarios within the extended and particle models and link the various outcomes with measurable biological parameters.

physics.bio-ph

Mechanical stress as a regulator of cell motility

The motility of a cell can be triggered or inhibited not only by an applied force but also by a mechanically neutral force couple. This type of loading, represented by an applied stress and commonly interpreted as either squeezing or stretching, can originate from extrinsic interaction of a cell with its neighbors. To quantify the effect of applied stresses on cell motility we use an analytically transparent one-dimensional model accounting for active myosin contraction and induced actin turnover. We show that stretching can polarize static cells and initiate cell motility while squeezing can symmetrize and arrest moving cells. We show further that sufficiently strong squeezing can lead to the loss of cell integrity. The overall behavior of the system depends on the two dimensionless parameters characterizing internal driving (chemical activity) and external loading (applied stress). We construct a phase diagram in this parameter space distinguishing between, static, motile and collapsed states. The obtained results are relevant for the mechanical understanding of contact inhibition and the epithelial-to-mesenchymal transition.

cond-mat.soft

Mechanics of motility initiation and motility arrest in crawling cells

Motility initiation in crawling cells requires transformation of a symmetric state into a polarized state. In contrast, motility arrest is associated with re-symmetrization of the internal configuration of a cell. Experiments on keratocytes suggest that polarization is triggered by the increased contractility of motor proteins but the conditions of re-symmetrization remain unknown. In this paper we show that if adhesion with the extra-cellular substrate is sufficiently low, the progressive intensification of motor-induced contraction may be responsible for both transitions: from static (symmetric) to motile (polarized) at a lower contractility threshold and from motile (polarized) back to static (symmetric) at a higher contractility threshold. Our model of lamellipodial cell motility is based on a 1D projection of the complex intra-cellular dynamics on the direction of locomotion. In the interest of analytical transparency we also neglect active protrusion and view adhesion as passive. Despite the unavoidable oversimplifications associated with these assumptions, the model reproduces quantitatively the motility initiation pattern in fish keratocytes and reveals a crucial role played in cell motility by the nonlocal feedback between the mechanics and the transport of active agents. A prediction of the model that a crawling cell can stop and re-symmetrize when contractility increases sufficiently far beyond the motility initiation threshold still awaits experimental verification.

physics.bio-ph