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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Fragile X mental retardation protein is necessary for neurotransmitter-activated protein translation at synapses
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Fragile X mental retardation protein is necessary for neurotransmitter-activated protein translation at synapses

机译：易碎的X智力低下蛋白对于突触中神经递质激活的蛋白翻译是必需的

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摘要

Fragile X mental retardation is caused by absence of the RNA-binding protein fragile X mental retardation protein (FMRP), encoded by the FMR1 gene. There is increasing evidence that FMRP regulates transport and modulates translation of some mRNAs. We studied neurotransmitter-activated synaptic protein synthesis in fmr1-knockout mice. Synaptoneurosomes from knockout mice did not manifest accelerated polyribosome assembly or protein synthesis as it occurs in wild-type mice upon stimulation of group I metabotropic glutamate receptors. Direct activation of protein kinase C did not compensate in the knockout mouse, indicating that the FMRP-dependent step is further along the signaling pathway. Visual cortices of young knockout mice exhibited a lower proportion of dendritic spine synapses containing polyribosomes than did the cortices of wild-type mice, corroborating this finding in vivo. This deficit in rapid neurotransmitter-controlled local translation of specific proteins may contribute to morphological and functional abnormalities observed in patients with fragile X syndrome.
机译：脆性X智力低下是由FMR1基因编码的RNA结合蛋白脆性X智力低下蛋白（FMRP）缺失引起的。越来越多的证据表明，FMRP调节运输并调节某些mRNA的翻译。我们研究了fmr1基因敲除小鼠中神经递质激活的突触蛋白合成。基因敲除小鼠的突触神经小体没有表现出加速的多核糖体装配或蛋白质合成，因为它在刺激I类代谢型谷氨酸受体后在野生型小鼠中发生。蛋白激酶C的直接激活在敲除小鼠中没有补偿，表明FMRP依赖性步骤进一步沿着信号传导途径进行。与野生型小鼠的皮质相比，年轻的基因敲除小鼠的视觉皮质显示出含有多核糖体的树突棘突触的比例更低，从而证实了这一发现。快速的神经递质控制的特定蛋白质局部翻译中的这种缺陷可能导致脆弱X综合征患者中观察到的形态和功能异常。

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