ArticleJournal of cell science2016
Epiboly generates the epidermal basal monolayer and spreads the nascent mammalian skin to enclose the embryonic body.
Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- A novel, PCP-dependent tissue organising principle coordinating morphogenesis between embryonic skin epidermal layers.Journal of anatomy · 2026Article
- Ventral body wall closure: Mechanistic insights from mouse models and translation to human pathology.Developmental dynamics : an official publication of the American Association of Anatomists · 2025Review
- Engineering tools for quantifying and manipulating forces in epithelia.Biophysics reviews · 2023Review
- Resolving morphogenesis into quantifiable cell behaviours.Development (Cambridge, England) · 2022Article
- Planar cell polarity proteins determine basal cell height in the later stage embryonic mouse epidermis'.Wellcome open research · 2022Article
- The expanding functional roles and signaling mechanisms of adhesion G protein-coupled receptors.Annals of the New York Academy of Sciences · 2019Article
- The role of Rho kinase (Rock) in re-epithelialization of adult zebrafish skin wounds.Small GTPases · 2018Article
- The Physical Basis of Coordinated Tissue Spreading in Zebrafish Gastrulation.Developmental cell · 2017Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Epiboly is a morphogenetic process that is employed in the surface ectoderm of anamniotes during gastrulation to cover the entire embryo. We propose here that mammals also utilise this process to expand the epidermis and enclose the body cavity and spinal cord with a protective surface covering. Our data supports a model whereby epidermal spreading is driven by the primary establishment of the epidermal basal progenitor monolayer through radial cell intercalation of a multi-layered epithelium towards the basal lamina. By using a suspension organotypic culture strategy, we find that this process is fibronectin-dependent and autonomous to the skin. The radial cell rearrangements that drive epidermal spreading also require ROCK activity but are driven by cell protrusions and not myosin II contractility. Epidermal progenitor monolayer formation and epidermal spreading are delayed in Crash mice, which possess a dominant mutation in Celsr1, an orthologue of the core planar cell polarity (PCP) Drosophila protein Flamingo (also known as Stan). We observe a failure of ventral enclosure in Crash mutants suggesting that defective epidermal spreading might underlie some ventral wall birth defects.
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Registered trials
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