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Misregulation of gene cohorts, which is caused by aberrant chromatin features and is observed in various cancers, has spurred the development and use of epigenetic anti-cancer drugs. Here, we argue that, in addition to small-molecule inhibitors that target chromatin regulators, synthetic reader-effectors that are recruited to abnormal chromatin features have the potential to correct gene misregulation in epigenetic therapy.
The long non-coding RNA Xist induces heterochromatinization of the X chromosome by recruiting repressive protein complexes to chromatin. Here we gather evidence, from the literature and from computational analyses, showing that Xist assemblies are similar in size, shape and composition to phase-separated condensates, such as paraspeckles and stress granules. Given the progressive sequestration of Xist’s binding partners during X-chromosome inactivation, we formulate the hypothesis that Xist uses phase separation to perform its function.
