Functional recapitulation of a likely evolutionary gain in gene expression shows that two genes are sufficient to switch mesoderm cell internalization from stochastic cell ingression to coordinated epithelial invagination.

A combination of two local cell interactions, intercalation and ingression amplified by a community-effect, is sufficient to explain the global movements of amniote gastrulation.

Elucidation of direct and indirect roles of GPCR signaling during gastrulation.

At gastrulation, mesoderm arises as a migratory germ layer that will participate to both foetal and placental development through region-dependant adaptation of cytoskeleton composition, cell shape and migration mode.

Micropatterned differentiation of mouse pluripotent stem cells gives rise to regionally distinct cell types arising in embryos at gastrulation.

The cellular behaviours that underlie the internalization of the multilayered endoderm anlage in Xenopus laevis link the ancestral mode of vertebrate gastrulation to common, epithelial-based mechanisms of gastrulation in non-vertebrate animals.

Expression of Pitx2c at the onset of gastrulation drives convergence and extension movements in the zebrafish embryo by promoting downstream pathways affecting chemokine signaling, integrin-ECM interactions, and planar cell polarity components.

Multipotent cardiac precursors within a population of mesoderm are rapidly fated to specific anatomic locations in the developing mouse heart.

In higher vertebrates, the position of the embryonic axis (the location at which gastrulation starts) is determined by the transcription factor Pitx2, which suggests that the mechanisms of this process, and hence those that regulate twinning, are related to those that set up the left–right axis.

Understanding the coordination of the forces generated in embryos by two processes, convergent extension and convergent thickening, is key to understanding how a hollow sphere of cells develops into an elongated embryo.