下颌骨发育畸形是人类最常见的先天性缺陷之一。本课题组发现FLRT3和BMP4在下颌胚基中的表达有重叠，在牙胚上皮也有FLRT3的表达；下颌髁突软骨细胞发生成骨诱导后，FLRT3的表达明显增强，其变化趋势与FGF2一致，与BMP2相反。据此，我们推测FLRT3可能通过FGF通路和BMP通路影响下颌骨生长发育。本研究拟通过沉默FLRT3基因，分别加入BMP阻断剂和FGF阻断剂，观察FLRT3与BMP和FGF信号通路的相互作用机制，以及对胚胎期下颌生长的影响；建立下颌髁突软骨细胞敲减和/或过表达FLRT3、Tbx2，干扰沉默转染FGF2、FGF8、BMP2、BMP4模型，研究FLRT3、Tbx2与FGF和BMP信号通路的相互作用机制。本研究的开展，将会深入了解颌面骨的生长发育，阐明FLRT3、FGF和BMP信号通路在下颌骨生长发育过程中的相互作用和调控机制，为先天性颌骨畸形的防治提供新的思路。

Mandibular disorders are among the most common birth defects in humans. Our research group found that the expression of FLRT3 and BMP4 overlapped in the mandibular blastocyst, and the expression of FLRT3 was also found in the tooth embryo epithelium. After osteogenic induction of mandibular condylar chondrocytes, the expression of FLRT3 was significantly increased, and the protein expression pattern of FLRT3 was closely related to FGF2 and BMP2 in different induction periods. Therefore, we speculated that FLRT3 may play an important role in the growth and development of mandible through FGF pathway and BMP pathway. In this study, the FLRT3 gene in chicken embryo was silenced by animal experiment and cell experiment, and BMP blocker and FGF blocker were added, respectively, to observe the interaction mechanism between FLRT3 and BMP and FGF signaling pathway, and the effect on mandible development in embryonic stage. FLRT3, Tbx2 knockdown and/or overexpression models were established, and FGF2, FGF8, BMP2 and BMP4 interference silencing transfection models were established to study the mechanism of FLRT3 and FGF/BMP signaling pathway, and to explore the signal network that FLRT3 is synergistically regulated by related factors during mandible development. This study will further understand maxillofacial development mechanism, and clarify the interaction and regulation mechanism of FLRT3, FGF and BMP signaling pathway in the growth and development of mandible, so as to provide new ideas for prevention and treatment of congenital maxillofacial malformation.