PUBLICATION
Antivin, a novel and divergent member of the TGFß superfamily, negatively regulates mesoderm induction
- Authors
- Thisse, C. and Thisse, B.
- ID
- ZDB-PUB-990106-23
- Date
- 1999
- Source
- Development (Cambridge, England) 126: 229-240 (Journal)
- Registered Authors
- Thisse, Bernard, Thisse, Christine
- Keywords
- antivin; mesoderm; inductin; TGFß; activin; zebrafish
- MeSH Terms
-
- Structure-Activity Relationship
- Zebrafish/embryology*
- Zebrafish/metabolism*
- Blastocyst/metabolism
- Mesoderm/metabolism*
- In Situ Hybridization
- Body Patterning/genetics
- RNA, Messenger/genetics
- Left-Right Determination Factors
- Activins
- Receptors, Growth Factor/metabolism
- Animals
- Gene Expression Regulation, Developmental/genetics*
- Amino Acid Sequence
- Inhibins/antagonists & inhibitors
- Activin Receptors
- Transforming Growth Factor beta/chemistry
- Transforming Growth Factor beta/genetics*
- Transforming Growth Factor beta/metabolism*
- Phenotype
- Molecular Sequence Data
- Embryo, Nonmammalian/metabolism
- Signal Transduction
- Cell Differentiation/genetics
- Zebrafish Proteins*
- PubMed
- 9847237 Full text @ Development
Citation
Thisse, C. and Thisse, B. (1999) Antivin, a novel and divergent member of the TGFß superfamily, negatively regulates mesoderm induction. Development (Cambridge, England). 126:229-240.
Abstract
Mesoderm induction and patterning are mediated by members of the TGFbeta superfamily. We have isolated a novel zebrafish member, antivin, that structurally is highly related to mouse lefty. Overexpression of antivin completely abolishes mesoderm induction at blastula stage, yet resultant embryos develop well-patterned epidermal and neural derivatives. The mesoderm-inhibiting activity of antivin can be mimicked by lefty and is suppressed by increasing levels of the mesodermal inducer Activin or its receptors. On the basis of its expression and activity, we propose that Antivin normally functions as a competitive inhibitor of Activin to limit mesoderm induction in the early embryo.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping