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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 syndrome: (What's) lost in translation?
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Fragile X syndrome: (What's) lost in translation?

机译：易碎X综合征：（什么）翻译中丢失了？

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摘要

The changing nature of synaptic function in neuronal dendrites during development is one of a myriad of phenomenological observations that have fascinated neuro-biologists for some time. In the case of fragile X syndrome (FXS), neurons exhibit long, spindly dendritic spines that appear to be morphologically immature (1). As with all dendritic spines, these FXR spines typically house elements of the postsynaptic density juxtaposed with components of the translation apparatus (2). A dominant mutation in the FMR1 gene gives rise to FXS through the elimination of FMR1 RNA. This gene encodes the fragile X mental retardation protein (FMRP), which is a RNA-bind-ing protein. By using in vitro assays, FMRP has been proposed to be involved in modulating translation through its binding to cellular RNAs and ribo-somes (3). In early studies, Weiler et al. (4) showed that the FMR1 RNA was localized in dendrites and that its translation could be modulated by group 1 metabotropic glutamate receptor (Gp1 mGluR) agonists. Subsequent studies have extended, and begun to clarify, the potential aftereffects of such events and their impact on normal cellular functioning, as well as FXS.
机译：发育过程中神经元树突状突触功能的变化性质是无数种使生物学家着迷一段时间的现象学观察之一。在脆性X综合征（FXS）的情况下，神经元表现出长而刺的树突棘，在形态上似乎不成熟（1）。与所有树突棘一样，这些FXR棘通常容纳突触后密度与平移设备（2）组件并列的元素。 FMR1基因的显性突变通过消除FMR1 RNA产生了FXS。该基因编码易碎的X智力低下蛋白（FMRP），它是一种RNA结合蛋白。通过使用体外测定，已提出FMRP通过与细胞RNA和核糖体结合而参与翻译调控（3）。在早期研究中，Weiler等人。 （4）表明FMR1 RNA定位于树突中，其翻译可能受第1组代谢型谷氨酸受体（Gp1 mGluR）激动剂的调节。随后的研究已经扩展并开始澄清此类事件的潜在后效应及其对正常细胞功能以及FXS的影响。

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