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

Most common genetic factors known to cause intellectual disability are Down syndrome and Fragile X syndrome. However, the underlying cellular and molecular mechan-isms of intellectual disability remain unclear. Recently, dendritic spine dysmorphogenesis and impaired local pro-tein 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 path-ways that regulate dendritic spine morphology and local protein synthesis