Gastruloids employ an alternative morphogenetic route to generate a posterior body axis on adherent substrates

Morphogenesis emerges from the integration of genetic programs with environmental signals, yet studying this interplay in embryos remains challenging due to the inherent complexity of embryonic systems, with their multiple interacting tissues and maternal influences. Using gastruloids as an accessible model, we systematically investigated how extracellular matrix composition directs morphogenetic strategies. We discovered that gastruloid substrate adhesion profiles evolve with differentiation state: while early aggregates attach only to laminin, mesoderm specification enables adhesion to fibronectin and collagens, possibly recapitulating sequential ECM deposition during embryogenesis. On laminin, gastruloids form flat structures with multiple radiating cell streams that maintain proper anterior-posterior gene expression patterns, demonstrating that gastruloids can elongate a patterned body axis using substrate-cell interactions instead of the cell-cell interactions seen in free-floating counterparts. Testing this through pharmacological inhibition of cytoskeletal components revealed unexpected substrate-specific requirements: blocking lamellipodia paradoxically enhanced cell-stream elongation, while blocking filopodia prevented its formation entirely. Crucially, these same inhibitors have no effect on free-floating gastruloids, demonstrating that tissues possess multiple, context-dependent routes to achieve axis elongation. Our findings establish that developing tissues harbour latent morphogenetic plasticity, and the ability to deploy alternative cellular mechanisms based on environmental context while preserving core developmental programs. This flexibility may provide insights into how evolution might explore morphological diversity without disrupting essential patterning, and suggests new strategies for controlling form in tissue engineering.