Embryonic Elongation controlled by Graded Cell Fate: A Molecular Dynamics Approach

TL;DR

This paper presents a computational model explaining how graded cell fate and motility drive embryonic elongation and node regression, aligning with experimental observations in avian embryos.

Contribution

It introduces a novel molecular dynamics simulation approach linking cell density and motility gradients to embryo elongation and regression mechanisms.

Findings

Model reproduces observed cell movement patterns.

Cell influx and motility gradients drive elongation and regression.

Simulations match experimental embryo phenotypes.

Abstract

Regression of Hensen's node from anterior to posterior is driving the elongation and patterning of avian embryo body. Recent experiments link gradient of presomitic mesoderm cell motility to displacement of the node and body axis elongation. Ingression of new cells into presomitic mesoderm tissue also contributes to the process. At present, movements of presomitic mesoderm can be tracked at single cell precision. Yet, mechanisms that couple these movements to regression and axis elongation are largely unknown. In this work we develop a computational approach to study regression of Hensen's node and the elongation of anterior-posterior body axis. Based on our simulations we propose that regression and the elongation are a result of the influx of new mesoderm cells mediated by cell density gradient. Addition of new cells leads to expansion of tissue in anterior-posterior direction (elongation) and pushes node towards posterior (regression). Motility gradient of cells further aids regression by biasing tissue expansion towards more motile posterior. We show that our model reproduces experimentally observed differences in presomitic mesoderm cell movements and regression of Hensen's node in various embryo phenotypes.