PUBLICATION
nkx2.3 is responsible for posterior pharyngeal cartilage formation by inhibiting Fgf signaling
- Authors
- Yang, S., Xu, X., Yin, Z., Liu, Y., Wang, H., Guo, J., Wang, F., Bao, Y., Zhang, T., Sun, S.
- ID
- ZDB-PUB-231201-6
- Date
- 2023
- Source
- Heliyon 9: e21915e21915 (Journal)
- Registered Authors
- Yang, Shuyan
- Keywords
- Differentiation, Fgf signaling, Posterior pharyngeal cartilages, Zebrafish, nkx2.3
- MeSH Terms
- none
- PubMed
- 38034615 Full text @ Heliyon
Citation
Yang, S., Xu, X., Yin, Z., Liu, Y., Wang, H., Guo, J., Wang, F., Bao, Y., Zhang, T., Sun, S. (2023) nkx2.3 is responsible for posterior pharyngeal cartilage formation by inhibiting Fgf signaling. Heliyon. 9:e21915e21915.
Abstract
Nkx2.3, a transcription factor, plays important roles in various developmental processes. However, the mechanisms underlying nkx2.3's regulation of pouch and pharyngeal arch development in zebrafish remain unclear. In this study, we demonstrated that knockdown or knockout of nkx2.3 resulted in the absence of posterior ceratobranchial cartilages in zebrafish. The absence of posterior pharyngeal cartilages is a consequence of the compromised proliferation and differentiation and survival of cranial neural crest cells (CNCCs). Notably, we found that nkx2.3 was not involved in endoderm pouch formation. Additionally, our findings suggested that nkx2.3 negatively regulated Fibroblast growth factor (Fgf) signaling, as overexpression of fgf8 could mimic the phenotype observed in nkx2.3 morphants, suppressing CNCC differentiation. Moreover, inhibiting Fgf signaling restored the abnormalities in posterior cartilages induced by nkx2.3 knockdown. These findings establish the essential role of nkx2.3 in the development of posterior ceratobranchial cartilages through the inhibition of fgf8.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping