Sp基因与Wnt基因对胚胎发育异常及唇腭裂的影响

正常的胚胎发育受不同的基因及相关信号通路的调控。近年来,同一组织中不同的基因与基因、基因与信号通路之间的关联性受到了国内外学者的广泛关注,Sp基因、Wnt基因的缺失或突变均可导致胚胎发育异常。本文综述结果表明:由于Sp基因缺失/突变导致的胚胎发育异常;锌指蛋白超家族成员Sp1-9参与了造血系统、呼吸系统、骨骼系统等多种组织器官的发育进程,它们的缺失或突变均可导致胚胎相应组织的发育异常,其中Sp8基因与腭裂的发生相关;通过总结近年来关于Wnt基因与唇腭裂的关系研究了解到Wnt3、Wnt3A、Wnt5A、Wnt9B、Wnt10A和Wnt11的表达异常与人类唇腭裂的发生密切相关;在胚胎发育过程中Sp5/8是Wnt信号通路的关键下游效应子,并且参与Wnt信号通路的组成。Sp5/8与Wnt信号通路共同参与调控胚胎期小鼠神经嵴的正常发育及胚胎干细胞的自我更新。综上所述,本文提出了Sp基因与Wnt基因可能共同参与调控胚胎期腭裂的形成及发生过程,同时为今后在腭裂模型中进一步研究二者之间的关联机制提供参考。

The effects of the Sp and Wnt genes on abnormalities in embryonic developmental and cleft lip and palate

Normal embryonic development is regulated by different genes and related signaling pathways. In recent years, the association between different genes and genes, genes and signaling pathways in the same organization has been widely concerned by scholars at home and abroad. Sp and Wnt gene deletion or mutation can lead to abnormal embryonic development. The results of this review indicate that abnormal embryonic development is due to Sp gene deletion/mutation The zinc finger protein superfamily member Sp1-9 is involved in the development of various tissues and organs, such as the hematopoietic system, respiratory system and skeletal system, and its deletion or mutation can lead to developmental abnormalities in embryonic tissues. In addition, the Sp8 gene is associated with the occurrence of cleft palate. By summarizing the observations about the relationship between the Wnt gene and cleft lip and palate in recent years, we can understand the abnormal expression of Wnt3, Wnt3A, Wnt5A, Wnt9B, Wnt10A and Wnt11 in humans.The occurrence of cleft lip and palate is closely related;Sp5/8 is a key downstream effector of the Wnt signaling pathway during embryonic development and participates in the Wnt signaling pathway. Sp5/8 and the Wnt signaling pathway are involved in the regulation of normal neural crest development and the self-renewal of embryonic stem cells in embryonic mice. In summary, this paper proposes that the Sp and Wnt genes may be involved in the regulation of the formation and occurrence of embryonic cleft palate and provides a reference for further study of the associated mechanisms between the two genes in the cleft palate model.