期刊
DEVELOPMENTAL CELL
卷 28, 期 6, 页码 617-632出版社
CELL PRESS
DOI: 10.1016/j.devcel.2014.02.011
关键词
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资金
- NIH predoctoral training grant [5T32GM066699-08]
- NIH [R37-AR27883]
- European Research Council starting grant [281903]
- European Research Council (ERC) [281903] Funding Source: European Research Council (ERC)
While gastrulation movements offer mechanistic paradigms for how collective cellular movements shape developing embryos, far less is known about coordinated cellular movements that occur later in development. Studying eyelid closure, we explore a case where an epithelium locally reshapes, expands, and moves over another epithelium. Live imaging, gene targeting, and cell-cycle inhibitors reveal that closure does not require overlying periderm, proliferation, or supracellular actin cable assembly. Laser ablation and quantitative analyses of tissue deformations further distinguish the mechanism from wound repair and dorsal closure. Rather, cell intercalations parallel to the tissue front locally compress it perpendicularly, pulling the surrounding epidermis along the closure axis. Functional analyses in vivo show that the mechanism requires localized myosin-IIA- and alpha 5 beta 1 integrin/fibronectin-mediated migration and E-cadherin downregulation likely stimulated by Wnt signaling. These studies uncover a mode of epithelial closure in which forces generated by cell intercalation are leveraged to tow the surrounding tissue.
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