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.
Highlights
GATA-binding protein 4 (GATA4) is a transcription factor that has been extensively studied in heart development and Edited by L
neural crest cells (NCCs)-derived craniofacial tissue using immunohistochemical analysis at E14.5, postnatal day 1 (P1), and P14 (Fig. 1a; detailed descriptions and magnified images of each panel can be found in the Supplementary Figure S1a–c)
GATA4 was expressed in the osteoblasts, and the positively stained cells were distributed along the surface of the bone trabecular (Supplementary Figure S1a)
Summary
GATA-binding protein 4 (GATA4) is a transcription factor that has been extensively studied in heart development and Edited by L. These authors contributed : Shuyu Guo, Yuxin Zhang. The development of neural crest cells (NCCs) can be broadly divided into three stages: formation, migration, and differentiation [9]. The inadequate development of NCCs during these stages may result in any of the aforementioned syndromes. The NC derivatives include bone and cartilage of the skull as well as tendons, muscles, and connective tissues of the ear, eye, teeth, and heart [5]. Due to their remarkable plasticity, the development of NCCs requires a complex landscape of transcriptional control [10]
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