PUBLICATION
Smad4 is required for the development of cardiac and skeletal muscle in zebrafish
- Authors
- Yang, J., Wang, J., Zeng, Z., Qiao, L., Zhuang, L., Jiang, L., Wei, J., Ma, Q., Wu, M., Ye, S., Gao, Q., Ma, D., Huang, X.
- ID
- ZDB-PUB-160802-5
- Date
- 2016
- Source
- Differentiation; research in biological diversity 92(4): 161-168 (Journal)
- Registered Authors
- Keywords
- Apoptosis, Development, Heart, Smad4, Trunk
- MeSH Terms
-
- Zebrafish/genetics
- Zebrafish/growth & development
- Myosin Light Chains/genetics
- Muscle, Skeletal/growth & development
- Gene Expression Regulation, Developmental
- Apoptosis/genetics
- Muscle Development/genetics*
- Cardiac Myosins/genetics
- Zebrafish Proteins/genetics*
- Cell Proliferation/genetics
- Animals
- Embryonic Development/genetics*
- Cell Differentiation/genetics*
- Transforming Growth Factor beta
- Heart/growth & development
- Smad4 Protein/genetics*
- PubMed
- 27477184 Full text @ Differentiation
Citation
Yang, J., Wang, J., Zeng, Z., Qiao, L., Zhuang, L., Jiang, L., Wei, J., Ma, Q., Wu, M., Ye, S., Gao, Q., Ma, D., Huang, X. (2016) Smad4 is required for the development of cardiac and skeletal muscle in zebrafish. Differentiation; research in biological diversity. 92(4):161-168.
Abstract
Transforming growth factor-beta (TGF-beta) regulates cellular functions and plays key roles in development and carcinogenesis. Smad4 is the central intracellular mediator of TGF-beta signaling and plays crucial roles in tissue regeneration, cell differentiation, embryonic development, regulation of the immune system and tumor progression. To clarify the role of smad4 in development, we examined both the pattern of smad4 expression in zebrafish embryos and the effect of smad4 suppression on embryonic development using smad4-specific antisense morpholino-oligonucleotides. We show that smad4 is expressed in zebrafish embryos at all developmental stages examined and that embryonic knockdown of smad4 results in pericardial edema, decreased heartbeat and defects in the trunk structure. Additionally, these phenotypes were associated with abnormal expression of the two heart-chamber markers, cmlc2 and vmhc, as well as abnormal expression of three makers of myogenic terminal differentiation, mylz2, smyhc1 and mck. Furthermore, a notable increase in apoptosis was apparent in the smad4 knockdown embryos, while no obvious reduction in cell proliferation was observed. Collectively, these data suggest that smad4 plays an important role in heart and skeletal muscle development.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping