Regenerative neurogenic response from glia requires insulin driven neuron-glia communication
Regenerative neurogenic response from glia requires insulin driven neuron-glia communication
复制标题
神经胶质细胞的再生神经反应需要胰岛素驱动的神经元-神经胶质细胞通讯
DOI：
10.1101/721498
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发表时间：
2019
期刊：
影响因子：
--
通讯作者：
Harrison N
中科院分区：
文献类型：
--
作者：
Harrison N
了解中枢神经系统损伤如何诱导动物的新生神经发生将有助于促进人类的再生。再生神经可能起源于胶质细胞，胶质细胞神经元-胶质细胞抗原2（NG 2）可能感知损伤诱导的神经元信号，但这些尚不清楚。在这里，我们用果蝇来寻找与NG 2同源物kon-tiki（kon）功能相关的基因，并鉴定了神经元分泌胰岛素所需的胰岛抗原-2（Ia-2）。fia-2的缺失和过度表达均诱导神经干细胞基因表达，损伤增加fia-2的表达并诱导异位神经干细胞。通过遗传分析和谱系追踪，我们证明Ia-2和Kon调节果蝇胰岛素样肽6（Dilp-6）诱导胶质细胞增殖和神经干细胞。异位神经干细胞可以分裂，并且有限的新生神经发生可以追溯到神经胶质细胞。总之，Ia-2和Dilp-6驱动神经元-胶质细胞中继，恢复胶质细胞并将胶质细胞重新编程为神经干细胞进行再生。
Understanding how injury to the central nervous system induces de novo neurogenesis in animals would help promote regeneration in humans. Regenerative neurogenesis could originate from glia and glial neuron-glia antigen-2 (NG2) may sense injury-induced neuronal signals, but these are unknown. Here, we usedDrosophilato search for genes functionally related to theNG2homologuekon-tiki (kon),and identifiedIslet Antigen-2 (Ia-2),required in neurons for insulin secretion. Both loss and over-expression ofia-2induced neural stem cell gene expression, injury increasedia-2expression and induced ectopic neural stem cells. Using genetic analysis and lineage tracing, we demonstrate that Ia-2 and Kon regulateDrosophilainsulin-like peptide 6 (Dilp-6) to induce glial proliferation and neural stem cells from glia. Ectopic neural stem cells can divide, and limited de novo neurogenesis could be traced back to glial cells. Altogether, Ia-2 and Dilp-6 drive a neuron-glia relay that restores glia and reprogrammes glia into neural stem cells for regeneration.