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Review
. 2018 Sep 24;373(1759):20170328.
doi: 10.1098/rstb.2017.0328.

The Same but Different: Cell Intercalation as a Driver of Tissue Deformation and Fluidity

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Free PMC article
Review

The Same but Different: Cell Intercalation as a Driver of Tissue Deformation and Fluidity

Robert J Tetley et al. Philos Trans R Soc Lond B Biol Sci. .
Free PMC article

Abstract

The ability of cells to exchange neighbours, termed intercalation, is a key feature of epithelial tissues. Intercalation is predominantly associated with tissue deformations that drive morphogenesis. More recently, however, intercalation that is not associated with large-scale tissue deformations has been described both during animal development and in mature epithelial tissues. This latter form of intercalation appears to contribute to an emerging phenomenon that we refer to as tissue fluidity-the ability of cells to exchange neighbours without changing the overall dimensions of the tissue. Here, we discuss the contribution of junctional dynamics to intercalation governing both morphogenesis and tissue fluidity. In particular, we focus on the relative roles of junctional contractility and cell-cell adhesion as the driving forces behind intercalation. These two contributors to junctional mechanics can be used to simulate cellular intercalation in mechanical computational models, to test how junctional cell behaviours might regulate tissue fluidity and contribute to the maintenance of tissue integrity and the onset of disease.This article is part of the Theo Murphy meeting issue 'Mechanics of development'.

Keywords: fluidity; intercalation; mechanics; morphogenesis; vertex model.

Conflict of interest statement

We have no competing interests.

Figures

Figure 1.
Figure 1.
Cell intercalation is associated both with tissue deformation and with tissues having static boundaries. (a) During an intercalation event, a junction shared between two cells (green) shrinks to a single point creating a four-way vertex. This vertex then resolves in the orthogonal direction as a new junction (magenta) grows. This results in an exchange of neighbours. In a tissue, there are often multiple intercalation events associated with either (b) tissue deformation or (c) no tissue deformation (old shrinking and new growing junctions are coloured as in (a)). We refer to the latter example (c) as ‘tissue fluidity’.
Figure 2.
Figure 2.
Polarized intercalation deforms tissues during morphogenesis. (a) Morphogenesis, particularly examples of convergent extension such as axis extension (here shown Drosophila GBE, germband in grey, direction of elongation shown by red arrow) and tubule elongation, is often driven by polarized cell intercalation. Intercalation can take the form of either a T1 process in a tetrad of cells or the formation and resolution of a multicellular rosette. In Drosophila, junction shrinkage (b) is driven by planar polarized distributions of myosin II and cadherin adhesion complexes. Cortical junctional myosin is enriched at DV-oriented shrinking junctions, while cadherin adhesion complexes are enriched at stable AP-oriented junctions. Junction shrinkage is further driven by pulsatile flows of medial myosin, which flow into shrinking junctions. To achieve new junction growth (c), junctional myosin II activity must be reduced in the growing junction. Junctions then grow owing to cell non-autonomous forces generated by medial myosin pulses in adjacent cells, close to the ends of the new junction.
Figure 3.
Figure 3.
Regulation of tissue fluidity in the Drosophila notum. A summary of experimental observations relating to the regulated tissue fluidity of the Drosophila notum (see text below schematics). This tissue can undergo a jamming transition from a fluid-like regime characterized by many intercalation events (left, shrinking junctions shown in green) and irregular packing to a solid-like regime with little intercalation and more regular hexagonal packing (right).
Figure 4.
Figure 4.
Vertex modelling of intercalation. (a) Schematic representation of vertex model cells (α) and junctions (ij). (b) Vertex model behaviours are determined by an energy function comprising three key terms: cell area elasticity, cell perimeter contractility and junction line tension. (c) Implementation of intercalation in vertex models. Intercalation can arise either by polarized line tension (top) or by fluctuations in line tension around a global mean (bottom). Line tension magnitudes are indicated by the thickness of green junctions. Old neighbours are in yellow, new neighbours in grey. Intercalations occur when junctions reach a threshold short length and the rearrangement induced by an intercalation reduces the total energy. (d) Summary of vertex model terms and parameters.

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