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Female mammals achieve dosage compensation by inactivating one of their two X chromosomes during development, a process entirely dependent on  Xist , an X-linked long non-coding RNA (lncRNA). At the onset of X chromosome inactivation (XCI),  Xist  is up-regulated and spreads along the future inactive X chromosome. Contextually, it recruits repressive histone and DNA modifiers that transcriptionally silence the X chromosome.  Xist  regulation is tightly coupled to differentiation and its expression is under the control of both pluripotency and epigenetic factors. Recent evidence has suggested that chromatin remodelers accumulate at the X Inactivation Center ( XIC ) and here we demonstrate a new role for Chd8 in  Xist  regulation in differentiating ES cells, linked to its control and prevention of spurious transcription factor interactions occurring within  Xist  regulatory regions. Our findings have a broader relevance, in the context of complex, developmentally-regulated gene expression.

Chd8 regulates X chromosome inactivation in mouse through fine-tuning control of Xist expression