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Biochemical and genetic interaction between the fragile X mental retardation protein and the microRNA pathway
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Biochemical and genetic interaction between the fragile X mental retardation protein and the microRNA pathway
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Journal Article
Biochemical and genetic interaction between the fragile X mental retardation protein and the microRNA pathway
2004
Overview
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.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ Animal Genetics and Genomics
/ Animals
/ Biomedical and Life Sciences
/ Drosophila Proteins - metabolism
/ Fragile X Syndrome - genetics
/ Fragile X Syndrome - metabolism
/ Genetics
/ Humans
/ Ligands
/ Male
/ microRNA
/ Microscopy, Electron, Scanning
/ miRNA
/ Nerve Tissue Proteins - genetics
/ Nerve Tissue Proteins - metabolism
/ Neuromuscular Junction - physiology
/ Neuromuscular Junction - ultrastructure
/ Neuronal Plasticity - genetics
/ Proteins
/ Ribonuclease III - metabolism
/ RNA
