PUBLICATION
Chordacentrum mineralization is delayed in zebrafish betaglycan-null mutants
- Authors
- Molina-Villa, T., Ramírez-Vidal, L., Mendoza, V., Escalante-Alcalde, D., López-Casillas, F.
- ID
- ZDB-PUB-210707-9
- Date
- 2021
- Source
- Developmental Dynamics : an official publication of the American Association of Anatomists 251(1): 213-225 (Journal)
- Registered Authors
- Lopez-Casillas, Fernando, Mendoza, Valentin, Ramirez-Vidal, Lizbeth
- Keywords
- none
- MeSH Terms
-
- Animals
- Receptors, Transforming Growth Factor beta*/genetics
- Receptors, Transforming Growth Factor beta*/metabolism
- Mice
- Zebrafish*/genetics
- Zebrafish*/metabolism
- Proteoglycans/genetics
- Transforming Growth Factor beta/genetics
- Transforming Growth Factor beta/metabolism
- Signal Transduction/genetics
- PubMed
- 34228380 Full text @ Dev. Dyn.
Citation
Molina-Villa, T., Ramírez-Vidal, L., Mendoza, V., Escalante-Alcalde, D., López-Casillas, F. (2021) Chordacentrum mineralization is delayed in zebrafish betaglycan-null mutants. Developmental Dynamics : an official publication of the American Association of Anatomists. 251(1):213-225.
Abstract
Background The Transforming Growth Factor β (TGFβ) family is a group of related proteins that signal through a type I and type II receptors. Betaglycan, also known as the type III receptor (Tgfbr3), is a co-receptor for various ligands of the TGFβ family that participates in heart, liver and kidney development as revealed by the tgfbr3-null mouse, as well as in angiogenesis as revealed by Tgfbr3 downregulation in morphant zebrafish.
Results Here we present CRISPR/Cas9-derived zebrafish Tgfbr3-null mutants, which exhibited unaltered embryonic angiogenesis and developed into fertile adults. One reproducible phenotype displayed by these Tgfbr3-null mutants is delayed chordacentra mineralization, which nonetheless does not result in vertebral abnormalities in the adult fishes. We also report that the canonical TGFβ signaling pathway is needed for proper chordacentra mineralization and that Tgfbr3 absence decreases this signal in the notochordal cells responsible for this process.
Conclusion Betaglycan's "ligand presentation" function contributes to the optimal TGFβ signaling required for zebrafish chordacentra mineralization. This article is protected by copyright. All rights reserved.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping