期刊
HELIYON
卷 9, 期 11, 页码 -出版社
CELL PRESS
DOI: 10.1016/j.heliyon.2023.e21915
关键词
Zebrafish; nkx2.3; Posterior pharyngeal cartilages; Differentiation; Fgf signaling
In this study, the researchers investigated the role of Nkx2.3 in the development of posterior ceratobranchial cartilages in zebrafish. They found that the absence of Nkx2.3 resulted in the absence of posterior pharyngeal cartilages, which was due to compromised proliferation, differentiation, and survival of cranial neural crest cells. The study also suggested that Nkx2.3 negatively regulated Fgf signaling and that inhibiting Fgf signaling could restore the abnormalities in posterior cartilages induced by Nkx2.3 knockdown.
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据