PUBLICATION
Regulation of hhex expression in the yolk syncytial layer, the potential Nieuwkoop center homolog in zebrafish
- Authors
- Bischof, J., and Driever, W.
- ID
- ZDB-PUB-041208-11
- Date
- 2004
- Source
- Developmental Biology 276(2): 552-562 (Journal)
- Registered Authors
- Bischof, Johannes, Driever, Wolfgang
- Keywords
- none
- MeSH Terms
-
- Nodal Protein
- Animals
- Signal Transduction/physiology
- Bone Morphogenetic Proteins/genetics
- Bone Morphogenetic Proteins/metabolism
- Organizers, Embryonic*
- Zebrafish/embryology*
- Zebrafish/genetics
- Bone Morphogenetic Protein 2
- Wnt Proteins
- Proteins/metabolism
- Gene Expression Regulation, Developmental*
- In Situ Hybridization
- Body Patterning*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- Transforming Growth Factor beta/genetics
- Transforming Growth Factor beta/metabolism
- Trans-Activators/metabolism
- Repressor Proteins/genetics
- Repressor Proteins/metabolism
- beta Catenin
- Homeodomain Proteins/genetics
- Homeodomain Proteins/metabolism*
- Egg Yolk*/cytology
- Egg Yolk*/metabolism
- Cytoskeletal Proteins/metabolism
- PubMed
- 15581885 Full text @ Dev. Biol.
Citation
Bischof, J., and Driever, W. (2004) Regulation of hhex expression in the yolk syncytial layer, the potential Nieuwkoop center homolog in zebrafish. Developmental Biology. 276(2):552-562.
Abstract
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping