Fragile X mental retardation protein modulates the fate of germline stem cells in Drosophila
Fragile X mental retardation protein modulates the fate of germline stem cells in Drosophila
复制标题
脆性 X 智力迟钝蛋白调节果蝇生殖干细胞的命运。
DOI：
10.1093/hmg/ddm129
复制
发表时间：
2007-08-01
影响因子：
3.5
通讯作者：
Jin, Peng
中科院分区：
文献类型：
--
作者：
Yang, Lele;Duan, Ranhui;Jin, Peng
脆性X综合征是一种常见的遗传性智力低下，是由脆性X智力低下蛋白（FMRP）的缺失引起的。FMRP不仅与特定的mrna和microRNAs （miRNA）相关，还与miRNA通路的组分相关，包括Dicer和Argonaute蛋白，它可能调节神经元的翻译。在果蝇中，dFmr1也参与生殖细胞和卵母细胞的规范；然而，是否需要dFmr1来控制生殖系干细胞（GSCs）的命运这个问题还没有答案。在这里，我们发现dFmr1是维持GSC和抑制分化所必需的。此外，我们发现在果蝇卵巢中，dFmr1蛋白与Argonaute蛋白1 （AGO1）相互作用，而AGO1是miRNA通路的关键组成部分。因此，dFmr1可能通过miRNA途径调节GSCs的命运。我们的结果提供了FMRP可能参与成体干细胞调控的第一个证据。
Fragile X syndrome, a common form of inherited mental retardation, is caused by the loss of fragile X mental retardation protein (FMRP). FMRP, which may regulate translation in neurons, associates not only with specific mRNAs and microRNAs (miRNA), but also with components of the miRNA pathway, including Dicer and Argonaute proteins. In Drosophila, dFmr1 is also known to be involved in germ cell and oocyte specification; however, the question of whether dFmr1 is required for controlling the fate of germline stem cells (GSCs) has gone unanswered. Here we show that dFmr1 is required for both GSC maintenance and repressing differentiation. Furthermore, we demonstrate that in Drosophila ovary, dFmr1 protein interacts with Argonaute protein 1 (AGO1), a key component of the miRNA pathway. Thus dFmr1 could modulate the fate of GSCs, likely via the miRNA pathway. Our results provide the first evidence that FMRP might be involved in the regulation of adult stem cells.