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Dev Biol January 1, 2018; 442 (1): 162-172.
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The b-HLH transcription factor Hes3 participates in neural plate border formation by interfering with Wnt/β-catenin signaling.

Hes3 belongs to the Hes basic helix-loop-helix family of transcriptional repressors that play central roles in maintaining progenitor cells and regulating binary cell fate decisions in the embryo. During Xenopus laevis development, hes3 is expressed in the embryonic ectoderm in a horseshoe shape domain at the edge of the developing neural pate. Hes3 mis-expression at early neurula stage blocks neural crest (snai2, sox8, sox9 and sox10) and cranial placode (six1 and dmrta1) gene expression, and promotes neural plate (sox2 and sox3) fate. At tailbud stage, these embryos exhibited a massive up-regulation of both sox8 and sox10 expression, associated with an increase in genes important for melanocytes differentiation (mitf and dct). Using a hormone inducible construct we show that Hes3 does not induce a pigment cell differentiation program de novo, rather it maintains progenitor cells in an undifferentiated state, and as Hes3 expression subsides overtime these cells adopt a pigment cell fate. We demonstrate that mechanistically Hes3 mediates its activity through inhibition of Wnt/β-catenin signaling, a molecular pathway critical for neural crest specification and pigment cell lineage differentiation. We propose that Hes3 at the edge of the neural plate spatially restricts the response to mesoderm-derived Wnt ligands, thereby contributing to the establishment of sharp boundaries of gene expression at the neural plate border.

PubMed ID: 30016640
PMC ID: PMC6138557
Article link: Dev Biol
Grant support: [+]

Species referenced: Xenopus laevis
Genes referenced: ctnnb1 dct dmrta1 foxd3 hes3 mitf nog npb pax3 runx1 six1 snai2 sox10 sox2 sox3 sox8 sox9 wnt8a zic1
GO keywords: neural crest cell fate specification [+]

Article Images: [+] show captions
References [+] :
Aoki, Sox10 regulates the development of neural crest-derived melanocytes in Xenopus. 2003, Pubmed, Xenbase