RESUMEN
We investigate the elasticity of an unsupported epithelial monolayer and we discover that unlike a thin solid plate, which wrinkles if geometrically incompatible with the underlying substrate, the epithelium may do so even in the absence of the substrate. From a cell-based model, we derive an exact elasticity theory and discover wrinkling driven by the differential apico-basal surface tension. Our theory is mapped onto that for supported plates by introducing a phantom substrate whose stiffness is finite beyond a critical differential tension. This suggests a new mechanism for an autonomous control of tissues over the length scale of their surface patterns.
RESUMEN
Epithelial furrowing is a fundamental morphogenetic process during gastrulation, neurulation, and body shaping. A furrow often results from a fold that propagates along a line. How fold formation and propagation are controlled and driven is poorly understood. To shed light on this, we study the formation of the cephalic furrow, a fold that runs along the embryo dorsal-ventral axis during Drosophila gastrulation and the developmental role of which is still unknown. We provide evidence of its function and show that epithelial furrowing is initiated by a group of cells. This cellular cluster works as a pacemaker, triggering a bidirectional morphogenetic wave powered by actomyosin contractions and sustained by de novo medial apex-to-apex cell adhesion. The pacemaker's Cartesian position is under the crossed control of the anterior-posterior and dorsal-ventral gene patterning systems. Thus, furrow formation is driven by a mechanical trigger wave that travels under the control of a multidimensional genetic guide.