UMR168 – Physico-Chimie Curie Lab

Team Publications

Year of publication 2018

Coscoy S, Baiz S, Octon J, Rhoné B, Perquis L, Tseng Q, Amblard F, Semetey V. (2018 Oct 16)

Microtopographies control the development of basal protrusions in epithelial sheets

Biointerphases : 13 : 041003 : DOI : 10.1116/1.5024601 Learn more
Summary

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Venzac B, Madoun R, Benarab T, Monnier S, Cayrac F, Myram S, Leconte L, Amblard F, Viovy JL, Descroix S, Coscoy S (2018 Oct 16)

Engineering small tubes with changes in diameter for the study of kidney cell organization

Biomicrofluidics : 12 : 024114 : DOI : 10.1063/1.5025027 Learn more
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Bipul R Acharya, Alexander Nestor-Bergmann, Xuan Liang, Shafali Gupta, Kinga Duszyc, Estelle Gauquelin, Guillermo A Gomez, Srikanth Budnar, Philippe Marcq, Oliver E Jensen, Zev Bryant, Alpha S Yap (2018 Oct 16)

A Mechanosensitive RhoA Pathway that Protects Epithelia against Acute Tensile Stress.

Developmental cell : DOI : S1534-5807(18)30776-7 Learn more
Summary

Adherens junctions are tensile structures that couple epithelial cells together. Junctional tension can arise from cell-intrinsic application of contractility or from the cell-extrinsic forces of tissue movement. Here, we report a mechanosensitive signaling pathway that activates RhoA at adherens junctions to preserve epithelial integrity in response to acute tensile stress. We identify Myosin VI as the force sensor, whose association with E-cadherin is enhanced when junctional tension is increased by mechanical monolayer stress. Myosin VI promotes recruitment of the heterotrimeric Gα12 protein to E-cadherin, where it signals for p114 RhoGEF to activate RhoA. Despite its potential to stimulate junctional actomyosin and further increase contractility, tension-activated RhoA signaling is necessary to preserve epithelial integrity. This is explained by an increase in tensile strength, especially at the multicellular vertices of junctions, that is due to mDia1-mediated actin assembly.

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Blanch-Mercader C., Yashunsky V., Garcia S., Duclos G., Giomi L., Silberzan P. (2018 Oct 9)

Turbulent dynamics of epithelial cell cultures

Phys. Rev. Lett. : 120 : 208001 : DOI : 10.1103/PhysRevLett.120.208101 Learn more
Summary

We investigate the large length and long time scales collective flows and structural rearrangements within in vitro human bronchial epithelial cell (HBEC) cultures. Activity-driven collective flows result in ensembles of vortices randomly positioned in space. By analyzing a large population of vortices, we show that their area follows an exponential law with a constant mean value and their rotational frequency is size independent, both being characteristic features of the chaotic dynamics of active nematic suspensions. Indeed, we find that HBECs self- organize in nematic domains of several cell lengths. Nematic defects are found at the interface between domains with a total number that remains constant due to the dynamical balance of nucleation and annihilation events. The mean velocity fields in the vicinity of defects are well described by a hydrodynamic theory of extensile active nematics.

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