Robust axis elongation by Nodal-dependent restriction of BMP signaling

Embryogenesis is brought about by the coordinated activities of different signaling pathways controlling cell fate specification and morphogenesis. In vertebrate gastrulation, both Nodal and BMP signaling play key roles in germ layer specification and morphogenesis, yet their interplay to coordinate embryo patterning with morphogenesis is still insufficiently understood. Here, we took a reductionist approach using zebrafish embryonic explants to study the coordination of Nodal and BMP signaling for embryo patterning and morphogenesis. We show that Nodal signaling not only triggers explant elongation by inducing mesendodermal progenitors but also by suppressing BMP signaling activity at the site of mesendoderm induction. Ectopic BMP signaling in the mesendoderm blocks cell alignment and oriented mesendoderm intercalations, key processes to drive explant elongation. Translating these ex vivo observations to the intact zebrafish embryo showed that, similar to explants, Nodal signaling renders the dorsal domain less sensitive towards BMP signaling to allow effective cell intercalations and thus robust embryonic axis elongation. These findings suggest a dual function of Nodal signaling in embryonic axis elongation by both inducing mesendoderm and maintaining low levels of BMP signaling activity in the dorsal portion of the mesendoderm.