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首页> 外文期刊>Cell discovery. >Ryk regulates Wnt5a repulsion of mouse corticospinal tract through modulating planar cell polarity signaling
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Ryk regulates Wnt5a repulsion of mouse corticospinal tract through modulating planar cell polarity signaling

机译：Ryk通过调节平面细胞极性信号传导调节小鼠皮质脊髓束的Wnt5a排斥

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It was previously reported a role for Ryk in mediating Wnt5a repulsion of the corticospinal tract (CST) in mice. Recent evidence has shown that Ryk regulates planar cell polarity (PCP) signaling through interacting with Vangl2. Here, in vivo , in vitro and biochemical analyses were applied to investigate the molecular cross-talk between the Ryk and PCP signaling pathways, revealing that PCP pathway components play important roles in CST anterior–posterior guidance. Ryk–Vangl2 interactions are crucial for PCP signaling to mediate Wnt5a repulsion of CST axons. Cytoplasmic distribution of Ryk is increased under high concentrations of Wnt5a and facilitates the cytoplasmic distribution of Vangl2, leading to inhibition of Frizzled3 translocation to cytoplasm. Alternatively, Ryk stabilizes Vangl2 in the plasma membrane under low Wnt5a concentrations, which promotes cytoplasmic translocation of Frizzled3. We propose that Ryk regulates PCP signaling through asymmetric modulation of Vangl2 distribution in the cytoplasm and plasma membrane, which leads to repulsion of CST axons in response to the Wnt gradient.
机译：以前有报道说Ryk在介导小鼠的皮质脊髓束（CST）的Wnt5a排斥中起作用。最近的证据表明，Ryk通过与Vangl2相互作用调节平面细胞极性（PCP）信号传导。在这里，通过体内，体外和生化分析研究了Ryk和PCP信号通路之间的分子串扰，揭示了PCP通路成分在CST前后导向中起着重要作用。 Ryk–Vangl2相互作用对于PCP信号传导介导Cnt轴突的Wnt5a排斥至关重要。在高浓度的Wnt5a下，Ryk的细胞质分布增加，并促进Vangl2的细胞质分布，从而导致Frizzled3易位至细胞质。或者，Ryk在低Wnt5a浓度下稳定质膜中的Vangl2，从而促进Frizzled3的胞质易位。我们建议Ryk通过对细胞质和质膜中的Vangl2分布进行不对称调节来调节PCP信号传导，从而响应Cnt轴突排斥Wnt梯度。

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