Interface extension is a continuum property suggesting a linkage between AP contractile and DV lengthening processes.

In the early embryo, the elongation of the anterior-posterior (AP) body axis is driven by cell intercalation in the germband epithelium. Neighboring cells intercalate through the contraction of AP interfaces (between AP neighbors) into higher-order vertices, which then resolve through the extension of new dorsal-ventral (DV) interfaces (between DV neighbors). Although interface contraction has been extensively studied, less is known about how new interfaces are established. Here we show that DV interface elongation behaviors initiate at the same time as AP contractions, and that DV interfaces which are newly created from resolution of higher-order vertices do not appear to possess a unique 'identity;' instead, all horizontal interfaces undergo lengthening, elongating through ratchetlike sliding behaviors analogous to those found in AP interfaces. Cortical F-actin networks are essential for high area oscillation amplitudes required for effective ratcheting. Our results suggest that, contrary to canonical models, the elongation of new DV interfaces is not produced by a mechanistically separate process. Instead, medial myosin populations drive oscillating radial forces in the cells to generate transient force asymmetries at all tricellular vertices, which-combined with planar polarized stabilization-produce directional ratcheted sliding to generate both AP interface contraction and DV interface elongation.