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首页> 外文期刊>Development >Pvr receptor tyrosine kinase signaling promotes post-embryonic morphogenesis, and survival of glia and neural progenitor cells in Drosophila
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Pvr receptor tyrosine kinase signaling promotes post-embryonic morphogenesis, and survival of glia and neural progenitor cells in Drosophila

机译：PVR受体酪氨酸激酶信号传导促进胚胎发生后的形态发生，并在果蝇中的胶质胶质生存和神经祖细胞

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摘要

Stem cells reside in specialized microenvironments, called niches, that regulate their development and the development of their progeny. However, the development and maintenance of niches are poorly understood. In the Drosophila brain, cortex glial cells provide a niche that promotes self-renewal and proliferation of neural stem cell-like cells (neuroblasts). In the central brain, neuroblasts and their progeny control post-embryonic morphogenesis of cortex glia through PDGF-like ligands, and this PDGFR receptor tyrosine kinase (RTK) signaling in cortex glia is required for expression of DE-cadherin, which sustains neuroblasts. Thus, through an RTK-dependent feed-forward loop, neuroblasts and their glial niche actively maintain each other. When the EGFR RTK is constitutively activated in cortex glia, they overexpress PDGF orthologs to stimulate autocrine PDGFR signaling, which uncouples their growth and survival from neuroblasts, and drives neoplastic glial transformation and elimination of neuroblasts. These results provide fundamental insights into glial development and niche regulation, and show that niche-neural stem cell feed-forward signaling becomes hijacked to drive neural tumorigenesis.
机译：干细胞位于特殊的微环境，称为利基，规范其发展和后代的发展。然而，利基的开发和维护很糟糕。在果蝇脑中，皮质胶质细胞提供了一种促进神经干细胞样细胞（神经细胞）的自我更新和增殖的利基。在中央脑，神经细胞和它们通过PDGF样配体的皮质胶质胶质细胞后胚胎形态发生，并且这种PDGFR受体酪氨酸激酶（RTK）信号传导在皮质胶质胶中，用于表达De-Cadherin，其维持神经细胞。因此，通过RTK依赖性前馈回路，神经细胞和它们的胶质性Niche主动保持彼此。当EGFR RTK在皮质胶质胶中组成型激活时，它们过度表达PDGF矫正器刺激自分泌PDGFR信号传导，其从神经细胞的生长和生存率渗透，并驱动肿瘤胶质转化和消除神经细胞的生存。这些结果为胶质发育和利基调控提供了基本的见解，并表明利基 - 神经干细胞前馈信令被劫持以驱动神经肿瘤瘤。

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