Cell Boundary Elongation by Non-autonomous Contractility in Cell Oscillation.

Throughout development, tissues exhibit dynamic cell deformation, which is characterized by the integration of cell boundary contraction and/or elongation. Such changes ultimately establish tissue morphology and function [1-5]. In comparison to cell boundary contraction, which is predominantly driven by non-muscle myosin II (MyoII)-dependent contraction [6-9], the mechanisms of cell boundary elongation remain elusive. We explored the dynamics of the amnioserosa, which is known to exhibit cell shape oscillation [10-15], as a model system to study the subcellular-level mechanics that spatiotemporally evolve during Drosophila dorsal closure. Here we show that cell boundary elongation occurs through a combination of a non-autonomous active process and an autonomous process. The former is driven by a transient change in the level of MyoII in the neighboring cells that pull the vertices, whereas the latter is governed by the relaxation of junctional tension. By monitoring cell boundary deformation during live imaging, junctional tension at the specific phase of cell boundary oscillation, e.g., contraction or elongation, was probed by laser ablation. Junctional tension during boundary elongation is lower than during the other phase of oscillation. We extended our tension measurements to non-invasively estimate a tension map across the tissue, and found a correlation between junctional tension and vinculin dynamics at the cell junction. We propose that the medial actomyosin network is used as an entity to both contract and elongate the cell boundary. Moreover, our findings raise a possibility that the level of vinculin at the cell boundary could be used to approximate junctional tension in vivo.