Epithelial invagination is a core component of the animal morphogenetic tool kit, transforming sheets of cells into cup-like structures in various embryonic contexts. In ascidians, marine invertebrate chordates that are closely related to vertebrates, gastrulation is initiated by invagination of the endoderm when just 10 endoderm precursor cells first apically constrict and then shorten along their apico-basal surfaces. Although some of the regulatory signals and mechanistic effectors of ascidian endoderm invagination have been identified, various aspects of its molecular control remain unclear, and are the focus of a new paper by Ulla-Maj Fiuza, Hitoyoshi Yasuo, Patrick Lemaire and colleagues. Using the ascidians Ciona and Phallusia, the authors first show that chemical inhibition of either Nodal or Eph signalling blocks endoderm invagination without affecting germ layer specification: cells apically constrict but fail to shorten, behaviours associated with a failure to switch from apical to baso-lateral accumulation of contractile Myosin II. They then uncover a signalling relay whereby Nodal signalling precedes and controls the level of expression of the Eph1 receptor in endoderm precursors. Finally, Eph signalling has an independent role in lengthening the cell cycle and inhibiting cell division until apico-basal shortening is completed. Thus, Nodal and Eph are two new and interlinked regulators of epithelial invagination in the early ascidian embryo.