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首页> 外文期刊>Neuron >Localized regulation of axonal RanGTPase controls retrograde injury signaling in peripheral nerve.
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Localized regulation of axonal RanGTPase controls retrograde injury signaling in peripheral nerve.

机译：轴突RanGTPase的局部调节控制周围神经的逆行损伤信号。

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摘要

Peripheral sensory neurons respond to axon injury by activating an importin-dependent retrograde signaling mechanism. How is this mechanism regulated? Here, we show that Ran GTPase and its associated effectors RanBP1 and RanGAP regulate the formation of importin signaling complexes in injured axons. A gradient of nuclear RanGTP versus cytoplasmic RanGDP is thought to be fundamental for the organization of eukaryotic cells. Surprisingly, we find RanGTP in sciatic nerve axoplasm, distant from neuronal cell bodies and nuclei, and in association with dynein and importin-alpha. Following injury, localized translation of RanBP1 stimulates RanGTP dissociation from importins and subsequent hydrolysis, thereby allowing binding of newly synthesized importin-beta to importin-alpha and dynein. Perturbation of RanGTP hydrolysis or RanBP1 blockade at axonal injury sites reduces the neuronal conditioning lesion response. Thus, neurons employ localized mechanisms of Ran regulation to control retrograde injury signaling in peripheral nerve.
机译：周围感觉神经元通过激活依赖于importin的逆行信号传导机制来响应轴突损伤。该机制如何监管？在这里，我们显示Ran GTPase及其相关效应子RanBP1和RanGAP调节受损轴突中importin信号复合物的形成。核仁RanGTP与细胞质RanGDP的梯度被认为是真核细胞组织的基础。出乎意料的是，我们在坐骨神经轴质中发现RanGTP，它远离神经元细胞体和细胞核，并与动力蛋白和importin-alpha相关。损伤后，RanBP1的局部翻译会刺激RanGTP从importins分离并随后水解，从而使新合成的importin-beta与importin-alpha和dynein结合。轴突损伤部位的RanGTP水解或RanBP1阻滞的摄动减少了神经元调节病变反应。因此，神经元利用Ran调节的局部机制来控制周围神经的逆行损伤信号传导。

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