alexa RalGTPase Controls Cell Polarity Organization during Ep
ISSN: 2168-9296

Cell & Developmental Biology
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Research Article

RalGTPase Controls Cell Polarity Organization during Epithelial Tissue Remodeling

Claire Beraud1, Yohanns Belaiche2, Jacques Camonis1 and Maria Balakireva1*
1Institut Curie, Inserm U830, 26 rue d’Ulm, 75005 Paris, France
2Institut Curie, CNRS UMR3215, Inserm U934, 26 rue d’Ulm, 75005 Paris, France
*Corresponding Author : Maria Balakireva
Institut Curie, Inserm U830, 26 rue d’Ulm, 75005 Paris, France
Tel: 33156246386
E-mail: [email protected]
Received February 14, 2014; Accepted March 19, 2014; Published March 21, 2014
Citation: Claire Beraud, Yohanns Belaiche, Jacques Camonis, Maria Balakireva (2014) RalGTPase Controls Cell Polarity Organization during Epithelial Tissue Remodeling. Cell Dev Biol 3:134. doi:10.4172/2168-9296.1000134
Copyright: © 2013 Beraud C, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 

Abstract

Ral, a Ras-like GTPase, is an essential component of Ras-driven oncogenesis that supports tumor initiation and progression. We explored the role of Ral in the polarity organization of epithelial tissue in Drosophila. We found that Ral is dispensable for the polarization of proliferative epithelial tissue, and that Ral is required for the maintenance of apical-basal polarity of post-mitotic epithelial cells during tissue remodeling. More precisely, lack of Ral activity results in loss of cortical apical aPKC and lateral Lgl, and in apical spreading and accumulation of Armadillo/betacatenin. Our analysis demonstrates that Ral regulates polarity organization by acting as a negative regulator of JNK and p38 MAPK signaling. Ral controls aPKC apical localization by down-regulating JNK and controls Armadillo localization at adherens junction by down-regulating p38 MAPK signaling, whereas Lgl membrane localization depends on both pathways. Finally, in the absence of Ral function aPKC becomes dispensable for Lgl basolateral localization and Armadillo is recruited to the cell membrane independently of DE-Cadherin and Bazooka localization. This suggests that additional mechanisms control Lgl and Arm distribution in polarized epithelia.

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