Ryk is a member of the receptor tyrosine kinase (RTK) family of proteins that control and regulate cellular processes. It is distinguished by binding Wnt ligands and having no detectable intrinsic protein tyrosine kinase activity suggesting Ryk is a pseudokinase. Here, we show an essential role for Ryk in directing morphogenetic events required for normal cardiac development through the examination of Ryk-deficient mice. We employed vascular corrosion casting, vascular perfusion with contrast dye, and immunohistochemistry to characterize cardiovascular and pharyngeal defects in Ryk^−/− embryos. Ryk^−/− mice exhibit a variety of malformations of the heart and outflow tract that resemble human congenital heart defects. This included stenosis and interruption of the aortic arch, ventriculoarterial malalignment, ventricular septal defects and abnormal pharyngeal arch artery remodelling. This study therefore defines a key intersection between a subset of growth factor receptors involved in planar cell polarity signalling, the Wnt family and mammalian cardiovascular development.

Ryk是控制和调节细胞过程的受体酪氨酸激酶（RTK）蛋白家族的成员。它的特征在于结合了Wnt配体，并且没有可检测的内在蛋白酪氨酸激酶活性，表明Ryk是一种假激酶。在这里，我们通过检查Ryk缺陷小鼠，显示Ryk在指导正常心脏发育所需的形态发生事件中的重要作用。我们采用血管腐蚀铸模，造影剂进行血管灌注以及免疫组织化学来表征Ryk ^-/-胚胎中的心血管和咽部缺损。雷克^-/- 小鼠表现出各种类似于人类先天性心脏缺陷的心脏和流出道畸形。这包括主动脉弓狭窄和中断，心室动脉错位，室间隔缺损和咽弓动脉异常重塑。因此，这项研究定义了参与平面细胞极性信号传导，Wnt家族和哺乳动物心血管发育的生长因子受体子集之间的关键交叉点。