PUBLICATION
Cell autonomous commitment to an endodermal fate and behaviour by activation of Nodal signalling
- Authors
- David, N.B. and Rosa, F.M.
- ID
- ZDB-PUB-011025-4
- Date
- 2001
- Source
- Development (Cambridge, England) 128(20): 3937-3947 (Journal)
- Registered Authors
- David, Nicholas, Rosa, Frederic
- Keywords
- endoderm; Nodal; fate determination; gastrulation; casanova; heart; zebrafish
- MeSH Terms
-
- Animals
- Cell Transplantation
- Endoderm/cytology
- Gastrula/cytology
- Heart/embryology
- High Mobility Group Proteins/genetics
- High Mobility Group Proteins/physiology
- Mutation
- Nodal Protein
- Protein Serine-Threonine Kinases*
- Receptors, Transforming Growth Factor beta/genetics
- Receptors, Transforming Growth Factor beta/physiology
- SOX Transcription Factors
- Signal Transduction
- Transcription Factors/genetics
- Transcription Factors/physiology
- Transforming Growth Factor beta/physiology*
- Zebrafish/embryology*
- Zebrafish/genetics
- Zebrafish/physiology
- Zebrafish Proteins*
- PubMed
- 11641218 Full text @ Development
Citation
David, N.B. and Rosa, F.M. (2001) Cell autonomous commitment to an endodermal fate and behaviour by activation of Nodal signalling. Development (Cambridge, England). 128(20):3937-3947.
Abstract
In vertebrates the endoderm germ layer gives rise to most tissues of the digestive tract and controls head and heart morphogenesis. The induction of endoderm development relies on extracellular signals related to Nodals and propagated intracellularly by TGFbeta type I receptors ALK4/Taram-A. It is unclear, however, whether Nodal/ALK4/Taram-A signalling is involved only in the specification of endodermal precursors or plays a more comprehensive role in the activation of the endodermal program leading to the irreversible commitment of cells to the endodermal fate. Using cell transplantation experiments in zebrafish, we show that marginal cells become committed to endoderm at the onset of gastrulation and that commitment to endoderm can be reached by intracellular activation of the Nodal pathway induced by expression of an activated form of the taram-A receptor, Tar*. In a manner similar to endoderm progenitors, Tar*-activated blastomeres translocate from their initial site of implantation in the blastoderm to reach the surface of their migration substratum, the yolk syncitial layer, where they join endogenous endodermal derivatives during gastrulation and differentiate according to their anteroposterior position. We demonstrate that Nodal/Tar*-induced commitment does not rely on a secondary signal released by Tar*-expressing cells or a signal released by endogenous endoderm since Tar*-expressing wild-type cells can restore endoderm derivatives when transplanted into the endoderm-deficient mutant casanova. Likewise, the YSL does not appear essential for the maintenance of endodermal identity during gastrulation once the Nodal pathway has been activated. Thus, our results demonstrate that the activation of Nodal signalling is sufficient to commit cells both to an endodermal fate and behaviour. Wild-type endoderm implantation into casanova embryos rescues, in a non-autonomous fashion, the defective fusion of the two heart primordia in the midline, highlighting the importance of endoderm for normal heart morphogenesis.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping