Abstract
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.
Highlights
Stem cells, which can self-renew and produce different cell types, are known to be regulated by both extrinsic signals and intrinsic factors [1]
Whether dFmr1 protein (dFmrp) could use specific miRNAs to regulate the fate of germline stem cells (GSCs) has remained unclear
We show that dFmrp is associated with specific microRNAs, including the bantam miRNA, in Drosophila ovary
Summary
Stem cells, which can self-renew and produce different cell types, are known to be regulated by both extrinsic signals and intrinsic factors [1]. In Drosophila ovary, a very small population of germline stem cells (GSCs) is maintained in a well-defined microenvironment, which provides an attractive system for investigating the regulatory mechanisms that determine the fate of stem cells [2,3]. The microRNA (miRNA) pathway was found to be required for controlling GSC self-renewal, since mutations in Dicer-1, Ago, and loquacious, which are involved in miRNA production and function in Drosophila, lead to rapid loss of GSCs [6,7,8,9]. MiRNAs could regulate gene expression through translational repression and mRNA degradation by binding to the 39 untranslated region (UTR) of their target mRNAs [10]. The specific miRNAs required for the regulation of GSC self-renewal and fate specification are yet to be determined
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