Article abstract
Nature Neuroscience 7, 113 - 117 (2004)
Published online: 4 January 2004 | doi:10.1038/nn1174
Biochemical and genetic interaction between the fragile X mental retardation protein and the microRNA pathway
Peng Jin1, Daniela C Zarnescu2, Stephanie Ceman1,3, Mika Nakamoto1, Julie Mowrey1, Thomas A Jongens4, David L Nelson5, Kevin Moses2 & Stephen T Warren1
Abstract
Fragile X syndrome is caused by a loss of expression of the fragile X mental retardation protein (FMRP). FMRP is a selective RNA-binding protein which forms a messenger ribonucleoprotein (mRNP) complex that associates with polyribosomes. Recently, mRNA ligands associated with FMRP have been identified. However, the mechanism by which FMRP regulates the translation of its mRNA ligands remains unclear. MicroRNAs are small noncoding RNAs involved in translational control. Here we show that in vivo mammalian FMRP interacts with microRNAs and the components of the microRNA pathways including Dicer and the mammalian ortholog of Argonaute 1 (AGO1). Using two different Drosophila melanogaster models, we show that AGO1 is critical for FMRP function in neural development and synaptogenesis. Our results suggest that FMRP may regulate neuronal translation via microRNAs and links microRNAs with human disease.
- Department of Human Genetics, Emory University, 615 Michael Street, Atlanta, Georgia 30322, USA.
- Department of Cell Biology, Emory University, 615 Michael Street, Atlanta, Georgia 30322, USA.
- Present address: Department of Cell and Structural Biology, University of Illinois, 601 S. Goodwin Avenue, Urbana, Illinois 61801, USA.
- Department of Genetics, University of Pennsylvania School of Medicine, 422 Curie Boulevard, Philadelphia, Pennsylvania 19104, USA.
- Department of Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA.
Correspondence to: Stephen T Warren1 e-mail: swarren@emory.edu
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