PUBLICATION
Overexpression of the transcriptional repressor FoxD3 prevents neural crest formation in Xenopus embryos
- Authors
- Pohl, B.S. and Knochel, W.
- ID
- ZDB-PUB-010521-1
- Date
- 2001
- Source
- Mechanisms of Development 103(1-2): 93-106 (Journal)
- Registered Authors
- Keywords
- none
- MeSH Terms
-
- Animals
- Repressor Proteins/biosynthesis*
- Repressor Proteins/genetics
- Repressor Proteins/physiology*
- Transcription, Genetic
- Down-Regulation
- In Situ Hybridization
- Molecular Sequence Data
- Sequence Homology, Amino Acid
- Protein Structure, Tertiary
- Cell Movement
- Xenopus/embryology*
- DNA-Binding Proteins*
- Recombinant Fusion Proteins/metabolism
- Neurons/metabolism
- Forkhead Transcription Factors
- Transcription Factors*
- Zebrafish Proteins*
- Time Factors
- Base Sequence
- Gene Expression Regulation, Developmental*
- Neural Crest/embryology*
- Xenopus Proteins*
- Phenotype
- Reverse Transcriptase Polymerase Chain Reaction
- Amino Acid Sequence
- PubMed
- 11335115 Full text @ Mech. Dev.
Citation
Pohl, B.S. and Knochel, W. (2001) Overexpression of the transcriptional repressor FoxD3 prevents neural crest formation in Xenopus embryos. Mechanisms of Development. 103(1-2):93-106.
Abstract
Xenopus FoxD3 (XFD-6) is an intron-less gene initially expressed within the Spemann organizer and later in premigratory neural crest cells. Based upon sequence and expression pattern comparisons, it represents the Xenopus orthologue to zebrafish fkd6, chicken CWH-3 and mammalian HFH-2 (genesis). Early expression of FoxD3 is activated by the Wnt-pathway and inhibited by BMP signalling. Ectopic overexpression of FoxD3 leads to an enlargement of the neural plate concomitant with a failure in neural crest formation, loss of anterior structures, lack of closure of the neural tube and severe defects in somitogenesis. Phenotypic variation is accompanied by down-regulation of neural crest markers, including Xslug, Xtwist and Xcadherin-11. FoxD3 also inhibits its own expression, thereby acting in a negative autoregulatory loop. By injections of VP16 and engrailed fusions we can demonstrate that FoxD3 acts as a negative transcriptional regulator; this repressive function strictly requires the presence of the winged helix domain. Transplantation experiments show that FoxD3 overexpressing cells from the prospective neural crest do neither differentiate nor migrate.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping