The bantam microRNA is associated with drosophila fragile X mental retardation protein and regulates the fate of germline stem cells.
The bantam microRNA is associated with drosophila fragile X mental retardation protein and regulates the fate of germline stem cells.
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Bantam microRNA 与果蝇脆性 X 智力迟钝蛋白相关并调节生殖干细胞的命运
DOI：
10.1371/journal.pgen.1000444
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发表时间：
2009-04
期刊：
影响因子：
4.5
通讯作者：
Chen D
中科院分区：
文献类型：
--
作者：
Yang Y;Xu S;Xia L;Wang J;Wen S;Jin P;Chen D
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。我们以前已经证明，dFmr1，果蝇直系同源的脆性X智力低下1基因，在果蝇卵巢生殖系干细胞的适当维护中发挥作用，然而，这背后的分子机制仍然难以捉摸。在这项研究中，我们使用了免疫沉淀试验，以揭示特定的microRNA（miRNA），特别是矮脚鸡的miRNA（矮脚鸡），与卵巢中的dFmrp物理相关。我们发现，像dFmr1，bantam不仅需要抑制原始生殖细胞的分化，它也作为一个外在因素的生殖系干细胞的维护。此外，我们发现矮脚鸡基因与dFmr1相互作用，以调节生殖系干细胞的命运。总的来说，我们的研究结果支持这样的观点，即FMRP介导的翻译途径通过特定的miRNA来控制干细胞调控。脆性X综合征是遗传性精神发育迟滞的最常见原因，其起因于功能性脆性X精神发育迟滞蛋白（FMRP）的缺失。FMRP是一种RNA结合蛋白，已知其与特定mRNA结合并在体外和体内调节其翻译。先前的研究表明FMRP是参与miRNA介导的翻译控制的miRNA途径的一个组分。在过去，我们发现，作为一个翻译调节，dFmrp可以调节果蝇干细胞的增殖和命运的规范，可能通过miRNA途径。然而，dFmrp是否可以使用特定的miRNA来调节GSC的命运仍不清楚。在这里，我们表明，dFmrp与特定的microRNAs（miRNA），包括矮脚鸡的miRNA，在果蝇卵巢。此外，我们表明，矮脚鸡基因与dFmr1相互作用，以调节GSC的命运。我们的研究结果表明，FMRP可以利用特定的miRNA来调节其mRNA靶点的翻译。
Fragile X syndrome, a common form of inherited mental retardation, is caused by the loss of fragile X mental retardation protein (FMRP). We have previously demonstrated that dFmr1, the Drosophila ortholog of the fragile X mental retardation 1 gene, plays a role in the proper maintenance of germline stem cells in Drosophila ovary; however, the molecular mechanism behind this remains elusive. In this study, we used an immunoprecipitation assay to reveal that specific microRNAs (miRNAs), particularly the bantam miRNA (bantam), are physically associated with dFmrp in ovary. We show that, like dFmr1, bantam is not only required for repressing primordial germ cell differentiation, it also functions as an extrinsic factor for germline stem cell maintenance. Furthermore, we find that bantam genetically interacts with dFmr1 to regulate the fate of germline stem cells. Collectively, our results support the notion that the FMRP-mediated translation pathway functions through specific miRNAs to control stem cell regulation. Fragile X syndrome, the most common cause of inherited mental retardation, results from the loss of functional Fragile X mental retardation protein (FMRP). FMRP is an RNA-binding protein and is known to bind to specific mRNAs and regulate their translation both in vitro and in vivo. Previous studies have suggested that FMRP is one component of the miRNA pathway involved in miRNA-mediated translational control. In the past we found that, as a translational regulator, dFmrp can modulate the proliferation and fate specification of stem cells in Drosophila, likely via the miRNA pathway. However, whether dFmrp could use specific miRNAs to regulate the fate of GSCs has remained unclear. Here, we show that dFmrp is associated with specific microRNAs (miRNAs), including the bantam miRNA, in Drosophila ovary. Furthermore, we show that bantam genetically interacts with dFmr1 to regulate the fate of GSCs. Our findings imply that FMRP could utilize specific miRNAs to regulate the translation of its mRNA targets.
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影响因子：
9.2
作者：
Jin, Zhigang;Xie, Ting
通讯作者：
Xie, Ting
影响因子：
16.2
作者：
Dockendorff, TC;Su, HS;Jongens, TA
通讯作者：
Jongens, TA
影响因子：
64.8
作者：
Hatfield, SD;Shcherbata, HR;Ruohola-Baker, H
通讯作者：
Ruohola-Baker, H
影响因子：
10.5
作者：
Caudy, AA;Myers, M;Hammond, SM
通讯作者：
Hammond, SM
DOI：
10.1083/jcb.200712159
发表时间：
2008-01-28
期刊：
The Journal of cell biology
影响因子：
--
作者：
Lin H
通讯作者：
Lin H