...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular brain >The planar cell polarity protein Vangl2 bidirectionally regulates dendritic branching in cultured hippocampal neurons
【24h】

The planar cell polarity protein Vangl2 bidirectionally regulates dendritic branching in cultured hippocampal neurons

机译：平面细胞极性蛋白Vangl2双向调节培养的海马神经元中的树突分支

获取原文
   

获取外文期刊封面封底 >>

       
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Background Van Gogh-like (Vangl) 2 is a planar cell polarity (PCP) protein that regulates the induction of polarized cellular and tissue morphology during animal development. In the nervous system, the core PCP signaling proteins have been identified to regulate neuronal maturation. In axonal growth cones, the antagonistic interaction of PCP components makes the tips of filopodia sensitive to guidance cues. However, the molecular mechanism by which the PCP signaling regulates spine and dendritic development remains obscure. Findings Here we explored the finding that a loss of function of Vangl2 results in a significant reduction in spine density and complexity of dendritic branching. In spite of a previous report, in which the Vangl2 C-terminal TSV motif was shown to be required for the interaction with PSD-95 and the C-terminal intracellular domain was shown to associate with N-cadherin, overexpression of deletion mutants (Vangl2-?TSV and Vangl2-?C) had little effect on spine density. However, when an N-terminal region deletion mutant was overexpressed, spine density was slightly down-regulated. Intriguingly, the deletion mutants had a more potent effect on dendritic branching, such that the deletion of the N-terminal region reduced dendritic branching, whereas deletion of the C-terminal region increased it. Conclusions Based on these results, Vangl2, a core PCP signaling pathway component, appears to have a functional role in neural complex formation. Especially in the case of dendritic branching, Vangl2 serves as a molecular hub to regulate neural morphology in opposite directions.
机译：背景梵高样（Vangl）2是一种平面细胞极性（PCP）蛋白，可调节动物发育过程中极化细胞和组织形态的诱导。在神经系统中，已经确定了核心PCP信号传导蛋白可调节神经元成熟。在轴突生长锥中，PCP组分的拮抗作用使丝状伪足的尖端对引导提示敏感。但是，PCP信号传导调节脊柱和树突发育的分子机制仍然不清楚。结果在这里，我们探索了Vangl2功能丧失导致脊柱密度显着降低和树枝状分支的复杂性的发现。尽管有先前的报道，其中显示Vangl2 C端TSV基序是与PSD-95相互作用所必需的，并且C端细胞内结构域显示与N-钙粘蛋白相关，但缺失突变体的过度表达（Vangl2 -ΔTSV和Vangl2-ΔC）对脊柱密度影响很小。但是，当N末端区域删除突变体过表达时，脊柱密度略有下调。有趣的是，缺失突变体对树突分支具有更有效的作用，因此N末端区域的缺失会降低树突分支，而C末端区域的缺失会增强其分支。结论基于这些结果，核心PCP信号通路成分Vangl2在神经复合物的形成中似乎具有功能性作用。特别是在树状分支的情况下，Vangl2充当分子枢纽，以相反方向调节神经形态。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号