Differential adhesion and actomyosin cable collaborate to drive Echinoid-mediated cell sorting

Chang, Li-Hsun; Chen, Peilong; Lien, Mong-Ting; Ho, Yu-Huei; Lin, Chiao-Ming; Pan, Yiting; Wei, Shu‐Yi; Hsu, Jui-Chou

doi:10.1242/dev.062257

Cited by 43 publications

(28 citation statements)

References 34 publications

(39 reference statements)

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“…6E,F). This is in line with findings that dominant-negative mutants of Ecad that lack adhesive properties downregulate the endogenous levels of full-length E-cad (Nieman et al, 1999;Troxell et al, 1999) through endocytosis and subsequent degradation (Chang et al, 2011). Importantly, analysis of single IL2R-E-cadCDHAtransfected cells in the context of untransfected neighbours revealed that 39.160.17% extruded compared with 4.560.9% of E-cadHA-transfected cells (Fig.…”

Section: Cleavage Of the E-cad Extracellular Domain Promotes Apical Csupporting

confidence: 89%

Extracellular cleavage of E-cadherin promotes epithelial cell extrusion

Grieve

Rabouille

2014

Journal of Cell Science

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BSTRACTEpithelial cell extrusion and subsequent apoptosis is a key mechanism to prevent the accumulation of excess cells. By contrast, when driven by oncogene expression, apical cell extrusion is followed by proliferation and represents an initial step of tumorigenesis. E-cadherin (E-cad), the main component of adherens junctions, has been shown to be essential for epithelial cell extrusion, but its mechanistic contribution remains unclear. Here, we provide clear evidence that cell extrusion can be driven by the cleavage of E-cad, both in a wild-type and an oncogenic environment. We first show that CDC42 activation in a single epithelial cell results in its efficient matrix metalloproteinase (MMP)-sensitive extrusion through MEK signalling activation and this is supported by E-cad cleavage. Second, using an engineered cleavable form of E-cad, we demonstrate that, by itself, truncation of extracellular E-cad at the plasma membrane promotes apical extrusion. We propose that extracellular cleavage of E-cad generates a rapid change in cell-cell adhesion that is sufficient to drive apical cell extrusion. Whereas in normal epithelia, extrusion is followed by apoptosis, when combined with active oncogenic signalling, it is coupled to cell proliferation.

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Section: Cleavage Of the E-cad Extracellular Domain Promotes Apical Csupporting

confidence: 89%

Extracellular cleavage of E-cadherin promotes epithelial cell extrusion

Grieve

Rabouille

2014

Journal of Cell Science

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“…Supra-cellular cables of MyoII have been previously associated with cell alignment in various epithelia (Nishimura et al, 2007;Simone and DiNardo, 2010;Walters et al, 2006) and have also been observed at the boundary of sorted clones, whereby cells align at a MyoII-enriched interface (Chang et al, 2011;Le Borgne et al, 2002;Wei et al, 2005). Interestingly, we find that the actomyosin cable defining the posterior boundary of the MF is also preferentially enriched for Rok, a component of the T1, MyoIIpositive AJ in the ventral epidermis (Simoes Sde et al, 2010).…”

Section: Compartment Boundary and Cell Intercalation During Retina Mosupporting

confidence: 72%

Atonal and EGFR signalling orchestraterok- andDrak-dependent adherens junction remodelling during ommatidia morphogenesis

et al. 2012

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SUMMARYMorphogenesis of epithelial tissues relies on the interplay between cell division, differentiation and regulated changes in cell shape, intercalation and sorting. These processes are often studied individually in relatively simple epithelia that lack the complexity found during organogenesis when these processes might all coexist simultaneously. To address this issue, we are making use of the developing fly retinal neuroepithelium. Retinal morphogenesis relies on a coordinated sequence of interdependent morphogenetic events that includes apical cell constriction, localized alignment of groups of cells and ommatidia morphogenesis coupled to neurogenesis. Here, we use live imaging to document the sequence of adherens junction (AJ) remodelling events required to generate the fly ommatidium. In this context, we demonstrate that the kinases Rok and Drak function redundantly during Myosin II-dependent cell constriction, subsequent multicellular alignment and AJ remodelling. In addition, we show that early multicellular patterning characterized by cell alignment is promoted by the conserved transcription factor Atonal (Ato). Further ommatidium patterning requires the epidermal growth factor receptor (EGFR) signalling pathway, which transcriptionally governs rok-and Drakdependent AJ remodelling while also promoting neurogenesis. In conclusion, our work reveals an important role for Drak in regulating AJ remodelling during retinal morphogenesis. It also sheds new light on the interplay between Ato, EGFR-dependent transcription and AJ remodelling in a system in which neurogenesis is coupled with cell shape changes and regulated steps of cell intercalation.

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“…Although the changes are distinct and depend on distinct molecular mechanisms, taking into account both clone boundary and bulk tensions is sufficient to account for their segregation from surrounding wt tissue. Although previous works demonstrated that cell cortical contractility or cell adhesion at the interface between two compartments, tissues or clones can promote their separation or contribute to tissue invagination (Graner, 1993;Le Borgne et al, 2002;Brodland, 2002;Wei et al, 2005;Laplante and Nilson, 2006;Landsberg et al, 2009;Monier et al, 2010;Chang et al, 2011;Aliee et al, 2012;Röper, 2012;Fagotto et al, 2013;Calzolari et al, 2014;Umetsu et al, 2014), our genetic and modeling findings show that Fig. 5.…”

Section: Discussioncontrasting

confidence: 57%

Modulation of junction tension by tumor-suppressors and proto-oncogenes regulates cell-cell contacts

et al. 2016

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Tumor suppressors and proto-oncogenes play crucial roles in tissue proliferation. Furthermore, de-regulation of their functions is deleterious to tissue architecture and can result in the sorting of somatic rounded clones minimizing their contact with surrounding wild-type (wt) cells. Defects in the shape of somatic clones correlate with defects in proliferation, cell affinity, cell-cell adhesion, oriented cell division and cortical contractility. Combining genetics, liveimaging, laser ablation and computer simulations, we aim to analyze whether distinct or similar mechanisms can account for the common role of tumor suppressors and proto-oncogenes in cell-cell contact regulation. In Drosophila epithelia, the tumor suppressors Fat (Ft) and Dachsous (Ds) regulate cell proliferation, tissue morphogenesis, planar cell polarity and junction tension. By analyzing the evolution over time of ft mutant cells and clones, we show that ft clones reduce their cell-cell contacts with the surrounding wt tissue in the absence of concomitant cell divisions and overproliferation. This contact reduction depends on opposed changes of junction tensions in the clone bulk and its boundary with neighboring wt tissue. More generally, either clone bulk or boundary junction tension is modulated by the activation of Yorkie, Myc and Ras, yielding similar contact reductions with wt cells. Together, our data highlight mechanical roles for proto-oncogene and tumor suppressor pathways in cell-cell interactions.

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Differential adhesion and actomyosin cable collaborate to drive Echinoid-mediated cell sorting

Cited by 43 publications

References 34 publications

Extracellular cleavage of E-cadherin promotes epithelial cell extrusion

Extracellular cleavage of E-cadherin promotes epithelial cell extrusion

Atonal and EGFR signalling orchestraterok- andDrak-dependent adherens junction remodelling during ommatidia morphogenesis

Modulation of junction tension by tumor-suppressors and proto-oncogenes regulates cell-cell contacts

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