Tension-oriented cell divisions limit anisotropic tissue tension in epithelial spreading during zebrafish epiboly
arXiv:1505.01642 · doi:10.1038/ncb2869
Abstract
Epithelial spreading is a common and fundamental aspect of various developmental and disease-related processes such as epithelial closure and wound healing. A key challenge for epithelial tissues undergoing spreading is to increase their surface area without disrupting epithelial integrity. Here we show that orienting cell divisions by tension constitutes an efficient mechanism by which the Enveloping Cell Layer (EVL) releases anisotropic tension while undergoing spreading during zebrafish epiboly. The control of EVL cell-division orientation by tension involves cell elongation and requires myosin II activity to align the mitotic spindle with the main tension axis. We also found that in the absence of tension-oriented cell divisions and in the presence of increased tissue tension, EVL cells undergo ectopic fusions, suggesting that the reduction of tension anisotropy by oriented cell divisions is required to prevent EVL cells from fusing. We conclude that cell-division orientation by tension constitutes a key mechanism for limiting tension anisotropy and thus promoting tissue spreading during EVL epiboly.
arXiv commentMethods, supplementary information and associated references are available in the published online version of the paper at http://www.nature.com/doifinder/10.1038/ncb2869
Cited by in corpus (9)
- Active wetting of epithelial tissues
- Cell division: a source of active stress in cellular monolayers
- Relating cell shape and mechanical stress in a spatially disordered epithelium using a vertex-based model
- Review: How dynamic prestress governs the shape of living systems, from the subcellular to tissue scale
- Unjamming and nematic flocks in endothelial monolayers during angiogenesis : theoretical and experimental analysis
- A model for boundary-driven tissue morphogenesis
- The Neoplasia as embryological phenomenon and its implication in the animal evolution and the origin of cancer. II. The neoplastic process as an evolutionary engine
- Elasticity and plasticity of epithelial gap closure
- Sensitive particle shape dependence of growth-induced mesoscale nematic structure