http://www.f1000biology.com/article/id/1086902/evaluation 。

评论内容如下：

人类FMR蛋白缺失会导致脆性X智力低下等疾病。这篇文章首次报道了果蝇中FMR蛋白的同源物参与调控果蝇原始生殖细胞和生殖干细胞的命运。作者利用果蝇突变体进行研究，揭示出果蝇dfmr基因对于抑制原始生殖细胞和生殖干细胞分化，维持生殖系细胞的正常功能非常重要；此外作者还表明果蝇的FMR蛋白还与调控microRNA信号通路的一种重要蛋白?Ago1蛋白存在相互作用。以上的研究成果将有助于人类dfmr基因突变女性卵巢早衰病症的研究。

This article is of special interest because it shows for the first time that dFmrp, a Drosophila protein homologous to human fragile X mental retardation protein (FMRP), the absence of which causes the fragile X syndrome, acts as a regulator of the fate of primordial germ cells (PGC), as well as germinal stem cells (GSC). Using dFMR1 mutants, the authors show that dFmrp acts as a repressor of both PGC and GSC differentiation, thus contributing to the maintenance of germline cells in Drosophila. dFmrp acts in conjunction with Ago1, a key component of the miRNA pathway regulating gene expression. Although not mentioned by the authors, their data could help in understanding the phenomenon of premature ovarian failure, observed in some women who are carriers of an FMR1 premutation.

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