Journal
HUMAN MOLECULAR GENETICS
Volume 16, Issue 15, Pages 1814-1820Publisher
OXFORD UNIV PRESS
DOI: 10.1093/hmg/ddm129
Keywords
-
Funding
- NIMH NIH HHS [R01 MH076090] Funding Source: Medline
- NINDS NIH HHS [R01 NS051630] Funding Source: Medline
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available