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Review
. 2020 Oct 12;375(1809):20190552.
doi: 10.1098/rstb.2019.0552. Epub 2020 Aug 24.

Cell intercalation in a simple epithelium

Affiliations
Review

Cell intercalation in a simple epithelium

Matteo Rauzi. Philos Trans R Soc Lond B Biol Sci. .

Abstract

Cell intercalation is a key topological transformation driving tissue morphogenesis, homeostasis and diseases such as cancer cell invasion. In recent years, much work has been undertaken to better elucidate the fundamental mechanisms controlling intercalation. Cells often use protrusions to propel themselves in between cell neighbours, resulting in topology changes. Nevertheless, in simple epithelial tissues, formed by a single layer of densely packed prism-shaped cells, topology change takes place in an astonishing fashion: cells exchange neighbours medio-laterally by conserving their apical-basal architecture and by maintaining an intact epithelial layer. Medio-lateral cell intercalation in simple epithelia is thus an exemplary case of both robustness and plasticity. Interestingly, in simple epithelia, cells use a combinatory set of mechanisms to ensure a topological transformation at the apical and basal sides. This article is part of the discussion meeting issue 'Contemporary morphogenesis'.

Keywords: E-cadherin adhesion; actomyosin flow; actomyosin tension; junction remodelling.

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Conflict of interest statement

I declare that I have no competing interests.

Figures

Figure 1.
Figure 1.
Cell intercalation in 2D and 3D. (a) Two-dimensional representation of cell intercalation. During intercalation a junction shrinks and a new junction forms and extends. During this process no gaps are formed. (b) Three-dimensional representation of cell intercalation. Cells start to intercalate from one end (e.g. from the apical side) forming scutoid shapes. Cell neighbour exchange then propagates from one end to the other, resolving cell intercalation. (Online version in colour.)
Figure 2.
Figure 2.
Mechanisms driving junction shrinkage. (a) Cortical tension model for junction shrinkage. (b) Medial actomyosin contraction model for junction shrinkage. Adapted with permission from Rauzi et al. [35]. (c) Differential anchorage model for actomyosin pulse flow. (d) Vertex sliding model for junction shrinkage. (e) Representation of a fundamental and a rosette intercalation event. (f) Basal–lateral protrusion model for cell intercalation initiation. Adapted with permission from Sun et al. [36]. (g) Representation of a columnar epithelial cell.
Figure 3.
Figure 3.
Contribution of cell intercalation to tissue pure shear. Tissue pure shear as a result of cell pure shear (top) or cell intercalation (bottom). (Online version in colour.)

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