Human Molecular Genetics Advance Access originally published online on May 21, 2007
Human Molecular Genetics 2007 16(15):1814-1820; doi:10.1093/hmg/ddm129
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Fragile X mental retardation protein modulates the fate of germline stem cells in Drosophila
1 State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, 2 Department of Human Genetics, Emory University School of Medicine, 615 Michael Street, Suite 301, Atlanta, GA 30322, USA and 3 Graduate School, Chinese Academy of Sciences, 25 Beisihuanxi Road, Haidian, Beijing 100080, P.R. China
* To whom correspondence should be addressed. Tel: +86 1064807325; Fax: +86 1064807318; Email: chendh{at}ioz.ac.cn; pjin{at}genetics.emory.edu
Received April 3, 2007; Accepted May 8, 2007
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.
The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors.