...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell Reports >Insulin-like Signaling Promotes Glial Phagocytic Clearance of Degenerating Axons through Regulation of Draper
【24h】

Insulin-like Signaling Promotes Glial Phagocytic Clearance of Degenerating Axons through Regulation of Draper

机译：胰岛素样信号通过Draper的调节促进神经胶质细胞的变性轴突清除。

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

摘要

Neuronal injury triggers robust responses from glial cells, including altered gene expression and enhanced phagocytic activity to ensure prompt removal of damaged neurons. The molecular underpinnings of glial responses to trauma remain unclear. Here, we find that the evolutionarily conserved insulin-like signaling (ILS) pathway promotes glial phagocytic clearance of degenerating axons in adult Drosophila. We find that the insulin-like receptor (InR) and downstream effector Akt1 are acutely activated in local ensheathing glia after axotomy and are required for proper clearance of axonal debris. InR/Akt1 activity, it is also essential for injury-induced activation of STAT92E and its transcriptional target draper, which encodes a conserved receptor essential for glial engulfment of degenerating axons. Increasing Draper levels in adult glia partially rescues delayed clearance of severed axons in glial InR-inhibited flies. We propose that ILS functions as a key post-injury communication relay to activate glial responses, including phagocytic activity.
机译：神经元损伤会触发神经胶质细胞的强烈反应，包括改变基因表达和增强吞噬活性，以确保迅速清除受损的神经元。胶质细胞对创伤反应的分子基础仍然不清楚。在这里，我们发现，在进化上保守的胰岛素样信号传导（ILS）途径促进成人果蝇中退化轴突的神经胶质吞噬清除。我们发现，胰岛素样受体（InR）和下游效应器Akt1在轴突切开后在局部包皮神经胶质细胞中被急性激活，是正确清除轴突碎片所必需的。 InR / Akt1活性对于损伤诱导的STAT92E及其转录靶受体的活化也很重要，后者编码一个对变性轴突的神经胶质吞噬至关重要的保守受体。成年神经胶质中Draper水平的提高部分可以挽救胶质InR抑制的果蝇中切断的轴突的延迟清除。我们建议ILS充当关键的损伤后通信中继，以激活神经胶质反应，包括吞噬活动。

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