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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.
