Cadherin clustering controls heterogeneous, asymmetric junction dynamics during vertebrate axis elongation

Tissue morphogenesis requires the control of physical forces by molecular patterning systems encoded in the genome. For example, tissue-level mechanical transformations in vertebrate embryos require the activity of cadherin adhesion proteins and the Planar Cell Polarity (PCP) signaling system. At the tissue level, collective cell movements are known to be highly complex, displaying combinations of fluid/solid behaviors, jamming transitions, and glass-like dynamics. The sub-cellular origin of these heterogeneous tissue dynamics is undefined. Here, high-speed super-resolution imaging and physical methods for quantifying motion revealed that the sub-cellular behaviors underlying vertebrate embryonic axis elongation display glass-like dynamic heterogeneities. A combination of theory and experiment demonstrates these behaviors are highly local, displaying asymmetries even within individual cell-cell junctions. Moreover, we demonstrate that these mechanical asymmetries require patterned lateral (cis-) clustering of cadherins that is dependent upon PCP signaling. These findings illuminate the mechanisms by which defined molecular patterning systems tune the mechanics of sub-cellular behaviors that drive vertebrate axis elongation.