ZFIN ID: ZDB-PUB-041208-11
Regulation of hhex expression in the yolk syncytial layer, the potential Nieuwkoop center homolog in zebrafish
Bischof, J., and Driever, W.
Date: 2004
Source: Developmental Biology   276(2): 552-562 (Journal)
Registered Authors: Bischof, Johannes, Driever, Wolfgang
Keywords: none
MeSH Terms:
  • Animals
  • Body Patterning*
  • Bone Morphogenetic Protein 2
  • Bone Morphogenetic Proteins/genetics
  • Bone Morphogenetic Proteins/metabolism
  • Cytoskeletal Proteins/metabolism
  • Egg Yolk*/cytology
  • Egg Yolk*/metabolism
  • Gene Expression Regulation, Developmental*
  • Homeodomain Proteins/genetics
  • Homeodomain Proteins/metabolism*
  • In Situ Hybridization
  • Nodal Protein
  • Organizers, Embryonic*
  • Proteins/metabolism
  • Repressor Proteins/genetics
  • Repressor Proteins/metabolism
  • Signal Transduction/physiology
  • Trans-Activators/metabolism
  • Transforming Growth Factor beta/genetics
  • Transforming Growth Factor beta/metabolism
  • Wnt Proteins
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
  • beta Catenin
PubMed: 15581885 Full text @ Dev. Biol.
The Nieuwkoop center is the earliest signaling center during dorsal-ventral pattern formation in amphibian embryos and has been implied to function in induction of the Spemann-Mangold organizer. In zebrafish, Nieuwkoop-center-like activity resides in the dorsal yolk syncytial layer (YSL) at the interface of the vegetal yolk cell and the blastoderm. hex homologs are expressed in the anterior endomesoderm in frogs (Xhex), the anterior visceral endoderm in mice, and the dorsal YSL in zebrafish (hhex). Here, we investigate the control of hhex expression in the YSL. We demonstrate that bozozok (boz) is absolutely required for early hhex expression, while overexpression of boz causes ectopic hhex expression. Activation of Wnt/beta-catenin signaling by LiCl induces hhex expression in wild-type YSL but not in boz mutant embryos, revealing that boz activity is required downstream of Wnt/beta-catenin signaling for hhex expression. Further, we show that the boz-mediated induction of hhex is independent of the Boz-mediated repression of bmp2b. Our data reveal that repressive effects of both Vega1 and Vega2 may be responsible for the exclusion of hhex expression from the ventral and lateral parts of the YSL. In summary, zebrafish hhex appears to be activated by Wnt/beta-catenin in the dorsal YSL, where Boz acts in a permissive way to limit repression of hhex by Vega1 and Vega2.