Nodal signaling regulates gastrulation cell behaviors largely in parallel with planar cell polarity signaling and is sufficient for ex vivo extension of embryonic explants.

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.

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.

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.

Phenotypic evolution can originate from variations in very precocious developmental events, starting even before fecundation, during the fabrication of the egg in the mother's gonad.

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