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首页> 外文期刊>Neuron >Loss of Dishevelleds Disrupts Planar Polarity in Ependymal Motile Cilia and Results in Hydrocephalus
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Loss of Dishevelleds Disrupts Planar Polarity in Ependymal Motile Cilia and Results in Hydrocephalus

机译：流失的丧失破坏了室间隔运动性纤毛的平面极性并导致脑积水

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摘要

Defects in ependymal (E) cells, which line the ventricle and generate cerebrospinal fluid flow through ciliary beating, can cause hydrocephalus. Dishevelled genes (Dvls) are essential for Wnt signaling, and Dvl2 has been shown to localize to the rootlet of motile cilia. Using the hGFAP-Cre;Dvl1-/-;2flox/flox;3+/- mouse, we show that compound genetic ablation of Dvls causes hydrocephalus. In hGFAP-Cre;Dvl1-/-;2flox/flox;3+/- mutants, E cells differentiated normally, but the intracellular and intercellular rotational alignments of ependymal motile cilia were disrupted. As a consequence, the fluid flow generated by the hGFAP-Cre;Dvl1-/-;2flox/flox;3+/- E cells was significantly slower than that observed in control mice. Dvls were also required for the proper positioning of motile cilia on the apical surface. Tamoxifen-induced conditional removal of Dvls in adult mice also resulted in defects in intracellular rotational alignment and positioning of ependymal motile cilia. These results suggest that Dvls are continuously required for E cell planar polarity and may prevent hydrocephalus.
机译：排列在心室并通过睫状跳动产生脑脊液流的室管膜（E）细胞缺陷会导致脑积水。杂乱的基因（Dvls）是Wnt信号转导必不可少的，并且Dvl2已显示定位于运动性纤毛的根部。使用hGFAP-Cre; Dvl1-/-; 2flox / flox; 3 +/-小鼠，我们显示Dvls的复合遗传消融导致脑积水。在hGFAP-Cre; Dvl1-/-; 2flox / flox; 3 +/-突变体中，E细胞正常分化，但室间隔运动性纤毛的细胞内和细胞间旋转排列被破坏。结果，hGFAP-Cre; Dvl1-/-; 2flox / flox; 3 +/- E细胞产生的流体流动明显慢于对照小鼠。还需要Dvl才能将活动性纤毛正确定位在根尖表面上。他莫昔芬诱导的成年小鼠Dvls的有条件去除也导致细胞内旋转排列和室管膜运动性纤毛定位的缺陷。这些结果表明，Dvls是E细胞平面极性的持续需要，并且可以预防脑积水。

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