Biochemical and genetic interaction between the fragile X mental retardation protein 3nd the microRNA pathway

Peng Jin, Daniela C. Zarnescu, Spephanie Ceman, Mika Nakamoto, Julie Mowrey, Thomas A. Jongens, David L. Nelson, Kevin Moses, Stephen T. Warren

Research output: Contribution to journalArticle

478 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)113-117
Number of pages5
JournalNature neuroscience
Volume7
Issue number2
DOIs
StatePublished - Feb 1 2004
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)

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    Jin, P., Zarnescu, D. C., Ceman, S., Nakamoto, M., Mowrey, J., Jongens, T. A., Nelson, D. L., Moses, K., & Warren, S. T. (2004). Biochemical and genetic interaction between the fragile X mental retardation protein 3nd the microRNA pathway. Nature neuroscience, 7(2), 113-117. https://doi.org/10.1038/nn1174