DSCR1 interacts with FMRP and is required for spine morphogenesis and local protein synthesis

Authors

  • Wei Wang,

    1. Department of Biology, Indiana University, Bloomington, IN, USA
    2. School of Nano-Bioscience and Chemical Engineering, UNIST (Ulsan National Institute of Science and Technology), Ulsan, Korea
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  • John Z Zhu,

    1. Department of Biology, Indiana University, Bloomington, IN, USA
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  • Karen T Chang,

    1. Department of Cell and Neurobiology, Zilkha Neurogenetic Institute, University of Southern California, Los Angeles, CA, USA
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  • Kyung-Tai Min

    Corresponding author
    1. Department of Biology, Indiana University, Bloomington, IN, USA
    2. School of Nano-Bioscience and Chemical Engineering, UNIST (Ulsan National Institute of Science and Technology), Ulsan, Korea
    • Corresponding author. School of Nano-Bioscience and Chemical Engineering, UNIST, Ulju gun, Eunyang Eup, Ulsan, Korea. Tel.:+82 52 217 2545; Fax:+82 52 217 2639; E-mail: ktaimin@unist.ac.kr

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  • There is a Have you seen? (September 2012) associated with this Article.

Abstract

Most common genetic factors known to cause intellectual disability are Down syndrome and Fragile X syndrome. However, the underlying cellular and molecular mechanisms of intellectual disability remain unclear. Recently, dendritic spine dysmorphogenesis and impaired local protein synthesis are posited to contribute to the cellular mechanisms of intellectual disability. Here, we show that Down syndrome critical region1 (DSCR1) interacts with Fragile X mental retardation protein (FMRP) and regulates both dendritic spine morphogenesis and local protein synthesis. Interestingly, decreasing the level of FMRP restores the DSCR1-induced changes in dendritic spine morphology. Our results imply that DSCR1 is a novel regulator of FMRP and that Fragile X syndrome and Down syndrome may share disturbances in common pathways that regulate dendritic spine morphology and local protein synthesis.

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