小分子RNA包括siRNAs,、miRNAs和piRNAs業(yè)已被證明在機體的發(fā)育過程中起著廣泛的調(diào)節(jié)作用。近年來的研究表明,，microRNA(miRNA)途徑參與調(diào)控果蠅生殖干細胞的增殖與分化,，如Dcr-1，Loquacious以及AGO1蛋白等miRNA途徑重要組分在決定干細胞命運中起關(guān)鍵作用,，但其作用機制仍不清楚,。
動物所陳大華研究組與Emory大學的金鵬實驗室前期合作結(jié)果證明了miRNA途徑另一個組分-dFmr1蛋白（編碼果蠅的FMRP蛋白）也參與果蠅生殖干細胞的命運調(diào)控。為了闡明dFmr1介導的miRNA途徑在果蠅生殖干細胞系統(tǒng)的作用機制,，該研究中,，作者采用免疫共沉淀的方法發(fā)現(xiàn)了一個名為Bantam的miRNA 小分子在卵巢中能夠和dFMR1蛋白特異相結(jié)合,。進一步研究作者發(fā)現(xiàn)，和dfmr1一樣,，bantam基因不僅是抑制原生殖細胞（PGCs）所必需的,，它也是作為一個外源因子來維持生殖干細胞（GSCs）的自我更新。此外,，作者發(fā)現(xiàn)bantam和dfmr1之間有遺傳上的相互作用,，并通過這種相互作用來調(diào)控GSCs的命運。本研究進一步證明了FMRP介導的翻譯抑制通路是通過特定的小RNA分子起作用來調(diào)控干細胞的行為,相關(guān)成果發(fā)表在最近出版的PLoS Genet上,。這項研究對揭示miRNA途徑調(diào)控干細胞行為的機制具有重要的指導意義,。（生物谷Bioon.com）
生物谷推薦原始出處：
PLoS Genet 5(4): e1000444. doi:10.1371/journal.pgen.1000444
The Bantam microRNA Is Associated with Drosophila Fragile X Mental Retardation Protein and Regulates the Fate of Germline Stem Cells
Yingyue Yang1#, Shunliang Xu2,3,4#, Laixin Xia1, Jun Wang1, Shengmei Wen1, Peng Jin2*, Dahua Chen1*
1 State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, People's Republic of China, 2 Department of Human Genetics, Emory University School of Medicine, Atlanta, Georgia, United States of America, 3 Department of Neurology, Second Hospital of Shandong University, Jinan, Shandong Province, People's Republic of China, 4 Department of Neurology, Qilu Hospital of Shandong University, Jinan, Shandong Province, People's Republic of China
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.
