Endodermal pouch-expressed dmrt2b is important for pharyngeal cartilage formation
Linwei Li,
Aihua Mao,
Peng Wang,
Guozhu Ning,
Yu Cao,
Qiang Wang
Affiliations
Linwei Li
State Key Laboratory of Membrane Biology, CAS Center for Excellence in Molecular Cell Science, Institute of Zoology, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Beijing 100101, China
Aihua Mao
State Key Laboratory of Membrane Biology, CAS Center for Excellence in Molecular Cell Science, Institute of Zoology, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Beijing 100101, China
Peng Wang
State Key Laboratory of Membrane Biology, CAS Center for Excellence in Molecular Cell Science, Institute of Zoology, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Beijing 100101, China
Guozhu Ning
State Key Laboratory of Membrane Biology, CAS Center for Excellence in Molecular Cell Science, Institute of Zoology, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Beijing 100101, China
Yu Cao
State Key Laboratory of Membrane Biology, CAS Center for Excellence in Molecular Cell Science, Institute of Zoology, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Beijing 100101, China
Qiang Wang
State Key Laboratory of Membrane Biology, CAS Center for Excellence in Molecular Cell Science, Institute of Zoology, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Beijing 100101, China
Pharyngeal pouches, a series of outpocketings derived from the foregut endoderm, are essential for craniofacial skeleton formation. However, the molecular mechanisms underlying endodermal pouch-regulated head cartilage development are not fully understood. In this study, we find that zebrafish dmrt2b, a gene encoding Doublesex- and Mab-3-related transcription factor, is specifically expressed in endodermal pouches and required for normal pharyngeal cartilage development. Loss of dmrt2b doesn't affect cranial neural crest (CNC) specification and migration, but leads to prechondrogenic condensation defects by reducing cxcl12b expression after CNC cell movement into the pharyngeal arches. Moreover, dmrt2b inactivation results in reduced proliferation and impaired differentiation of CNC cells. We also show that dmrt2b suppresses crossveinless 2 expression in endodermal pouches to maintain BMP/Smad signaling in the arches, thereby facilitating CNC cell proliferation and chondrogenic differentiation. This work provides insight into how transcription factors expressed in endodermal pouches regulate pharyngeal skeleton development through tissue–tissue interactions.