Rectified random cell motility as a mechanism for embryo elongation

The body of vertebrate embryos forms by posterior elongation from a terminal growth zone called the tail bud. The tail bud is a source of highly motile cells that eventually constitute the presomitic mesoderm (PSM), a tissue that plays an important role in elongation movements. PSM cells establish an anterior-posterior cell motility gradient that parallels a gradient associated with the degradation of a specific cellular signal (FGF) known to be implicated in cell motility. Here, we combine the electroporation of fluorescent reporters in the PSM with time-lapse imaging in the chicken embryo to quantify cell diffusive movements along the motility gradient. We show that a simple microscopic model for random cell motility induced by FGF activity along with geometric confinement leads to rectified tissue elongation consistent with our observations. A continuum analog of the microscopic model leads to a macroscopic mechano-chemical model for tissue extension that couples FGF activity-induced cell motility and tissue rheology, and is consistent with the experimentally observed speed and extent of elongation. Together, our experimental observations and theoretical models explain how the continuous addition of cells at the tail bud combined with lateral confinement can be converted into oriented movement and drive body elongation.

Automated summary

This study investigates the effects of cell motility gradients on body elongation using the chicken embryo as a model. The combination of electroporation and time-lapse imaging techniques reveals that random cell motility induced by a cellular signal (FGF) and geometric confinement play important roles in tissue elongation. Both experimental observations and theoretical models demonstrate that the continuous addition of cells at the tail bud, combined with lateral confinement, results in directed movement and body elongation.