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Sox2 acts as a rheostat of epithelial to mesenchymal transition during neural crest development


Mandalos, Nikolaos; Rhinn, Muriel; Granchi, Zoraide; Karampelas, Ioannis; Mitsiadis, Thimios A; Economides, Aris N; Dollé, Pascal; Remboutsika, Eumorphia (2014). Sox2 acts as a rheostat of epithelial to mesenchymal transition during neural crest development. Frontiers in Physiology:5:345.

Abstract

Precise control of self-renewal and differentiation of progenitor cells into the cranial neural crest (CNC) pool ensures proper head development, guided by signaling pathways such as BMPs, FGFs, Shh and Notch. Here, we show that murine Sox2 plays an essential role in controlling progenitor cell behavior during craniofacial development. A “Conditional by Inversion” Sox2 allele (Sox2COIN) has been employed to generate an epiblast ablation of Sox2 function (Sox2EpINV). Sox2EpINV/+(H) haploinsufficient and conditional (Sox2EpINV/mosaic) mutant embryos proceed beyond gastrulation and die around E11. These mutant embryos exhibit severe anterior malformations, with hydrocephaly and frontonasal truncations, which could be attributed to the deregulation of CNC progenitor cells during their epithelial to mesenchymal transition. This irregularity results in an exacerbated and aberrant migration of Sox10+ NCC in the branchial arches and frontonasal process of the Sox2 mutant embryos. These results suggest a novel role for Sox2 as a regulator of the epithelial to mesenchymal transitions (ΕΜΤ) that are important for the cell flow in the developing head.

Abstract

Precise control of self-renewal and differentiation of progenitor cells into the cranial neural crest (CNC) pool ensures proper head development, guided by signaling pathways such as BMPs, FGFs, Shh and Notch. Here, we show that murine Sox2 plays an essential role in controlling progenitor cell behavior during craniofacial development. A “Conditional by Inversion” Sox2 allele (Sox2COIN) has been employed to generate an epiblast ablation of Sox2 function (Sox2EpINV). Sox2EpINV/+(H) haploinsufficient and conditional (Sox2EpINV/mosaic) mutant embryos proceed beyond gastrulation and die around E11. These mutant embryos exhibit severe anterior malformations, with hydrocephaly and frontonasal truncations, which could be attributed to the deregulation of CNC progenitor cells during their epithelial to mesenchymal transition. This irregularity results in an exacerbated and aberrant migration of Sox10+ NCC in the branchial arches and frontonasal process of the Sox2 mutant embryos. These results suggest a novel role for Sox2 as a regulator of the epithelial to mesenchymal transitions (ΕΜΤ) that are important for the cell flow in the developing head.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Center for Dental Medicine > Institute of Oral Biology
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:22 August 2014
Deposited On:26 Aug 2014 16:10
Last Modified:05 Aug 2017 08:23
Publisher:Frontiers Research Foundation
ISSN:1664-042X
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:https://doi.org/10.3389/fphys.2014.00345
PubMed ID:25309446

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