Fragile X mental retardation protein (FMRP) represses the transcription of many target genes, including genes that encode chromatin-associated proteins. Loss of FMRP leads to fragile X syndrome (FXS); however, whether misregulation of chromatin-associated proteins contributes to FXS is unclear. Korb et al. showed that neurons from mice that lack FMRP have increased levels of several chromatin-associated proteins, including bromodomain-containing protein 4 (BRD4). Inhibition of BRD4 using the small molecule JQ1 reversed many of the gene expression changes observed in the FMRP-null neurons, and rescued memory and social deficits in FXS mice.
References
Korb, E. et al. Excess translation of epigenetic rgulators contributes to fragile X syndrome and is alleviated by Brd4 inhibition. Cell http://dx.doi.org/10.1016/j.cell.2017.07.033 (2017)
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Bray, N. A transcription-targeting target. Nat Rev Neurosci 18, 572 (2017). https://doi.org/10.1038/nrn.2017.123
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DOI: https://doi.org/10.1038/nrn.2017.123
