We report that Foxc2-/- embryos on the 129s6/SvEv inbred genetic background display persistent truncus arteriosus and hypoplastic ventricles before embryonic lethality. Foxc2 loss-of-function resulted in perturbed cardiac neural crest cell migration and their reduced contribution to the outflow tract as evidenced by lineage tracing analyses together with perturbed expression of the neural crest cell markers Sox10 and Crabp1. Foxc2 loss-of-function also resulted in alterations in PlexinD1, Twist1, PECAM1, and Hand1/2 expression in association with vascular and ventricular defects.
Our data indicate Foxc2 is required for proper migration of cardiac neural crest cells, septation of the outflow tract, and development of the ventricles. Developmental Dynamics 247:1286-1296, 2018. © 2018 Wiley Periodicals, Inc.
我们报告说,129s6/SvEv近交遗传背景上的Foxc2-/-胚胎在胚胎致死之前表现出持续的动脉干和发育不良的心室。Foxc2功能丧失导致心脏神经c细胞迁移受到干扰,并且它们对流出道的贡献减少,如谱系追踪分析以及神经c细胞标记物Sox10和Crabp1的表达受到干扰所证明。Foxc2功能丧失还导致与血管和心室缺陷相关的PlexinD1、Twist1、PECAM1和Hand1/2表达的改变。
我们的数据表明Foxc2是心脏神经c细胞正常迁移所必需的,流出道的分隔,和心室的发育。发展动态247:1286-1296,2018。©2018Wiley期刊,Inc.