PUBLICATION
GATA4 as a novel regulator involved in the development of the neural crest and craniofacial skeleton via Barx1
- Authors
- Guo, S., Zhang, Y., Zhou, T., Wang, D., Weng, Y., Chen, Q., Ma, J., Li, Y.P., Wang, L.
- ID
- ZDB-PUB-180311-1
- Date
- 2018
- Source
- Cell death and differentiation 25(11): 1996-2009 (Journal)
- Registered Authors
- Keywords
- none
- MeSH Terms
-
- Animals
- Cell Proliferation
- Facial Bones/diagnostic imaging
- Facial Bones/growth & development*
- Facial Bones/metabolism
- Female
- GATA4 Transcription Factor/antagonists & inhibitors
- GATA4 Transcription Factor/genetics
- GATA4 Transcription Factor/metabolism*
- Gene Expression Regulation, Developmental
- Homeodomain Proteins/genetics
- Homeodomain Proteins/metabolism*
- Male
- Mice
- Mice, Inbred C57BL
- Neural Crest/cytology
- Neural Crest/growth & development*
- Neural Crest/metabolism
- Nuclear Proteins/genetics
- Nuclear Proteins/metabolism
- Promoter Regions, Genetic
- Protein Binding
- RNA Interference
- RNA, Messenger/metabolism
- RNA, Small Interfering/metabolism
- SOX9 Transcription Factor/genetics
- SOX9 Transcription Factor/metabolism
- Transcription Factors/genetics
- Transcription Factors/metabolism*
- Twist-Related Protein 1/genetics
- Twist-Related Protein 1/metabolism
- X-Ray Microtomography
- Zebrafish/metabolism
- PubMed
- 29523871 Full text @ Cell Death Differ.
Citation
Guo, S., Zhang, Y., Zhou, T., Wang, D., Weng, Y., Chen, Q., Ma, J., Li, Y.P., Wang, L. (2018) GATA4 as a novel regulator involved in the development of the neural crest and craniofacial skeleton via Barx1. Cell death and differentiation. 25(11):1996-2009.
Abstract
The role of GATA-binding protein 4 (GATA4) in neural crest cells (NCCs) is poorly defined. Here we showed that mouse NCCs lacking GATA4 exhibited developmental defects in craniofacial bone, teeth, and heart. The defects likely occurred due to decreased cell proliferation at the developmental stage. The in vitro results were consistent with the mouse model. The isobaric tags for relative and absolute quantitation assay revealed that BARX1 is one of the differentially expressed proteins after GATA4 knockdown in NCCs. On the basis of the results of dual-luciferase, electro-mobility shift, and chromatin immunoprecipitation assays, Barx1 expression is directly regulated by GATA4 in NCCs. In zebrafish, gata4 knockdown affects the development of NCCs derivatives. However, the phenotype in zebrafish could be partly rescued by co-injection of gata4 morpholino oligomers and barx1 mRNA. This study identified new downstream targets of GATA4 in NCCs and uncovered additional evidence of the complex regulatory functions of GATA4 in NCC development.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping