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Summary
Fragile X syndrome (FXS) is the most prevalent inherited form of intellectual disability and autism (1). FXS is usually caused by transcriptional silencing of the fragile X mental retardation 1 (FMR1) gene, which encodes fragile X mental retardation protein (FMRP), an RNA-binding protein that is thought to repress the translation of specific messenger RNAs (mRNAs). Precise translational control is especially critical in neurons because rapid synthesis of proteins from preexisting mRNAs underlies many forms of synaptic plasticity, which is altered in animal models of FXS (2). Progress has been made in identifying RNAs that FMRP binds, but its functional targets and modes of translational control remain elusive, especially during development (3–7). On page 709 of this issue, Greenblatt and Spradling (8) use Drosophila melanogaster oocytes to demonstrate that FMRP increases the translation of multiple long mRNAs, many of which are implicated in intellectual disability and autism.
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