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Hijacking of transcriptional condensates by endogenous retroviruses. 2022
Vahid Asimi, and
Abhishek Sampath Kumar, and
Henri Niskanen, and
Christina Riemenschneider, and
Sara Hetzel, and
Julian Naderi, and
Nina Fasching, and
Niko Popitsch, and
Manyu Du, and
Helene Kretzmer, and
Zachary D Smith, and
Raha Weigert, and
Maria Walther, and
Sainath Mamde, and
David Meierhofer, and
Lars Wittler, and
René Buschow, and
Bernd Timmermann, and
Ibrahim I Cisse, and
Stefan L Ameres, and
Alexander Meissner, and
Denes Hnisz
Department of Genome Regulation, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Most endogenous retroviruses (ERVs) in mammals are incapable of retrotransposition; therefore, why ERV derepression is associated with lethality during early development has been a mystery. Here, we report that rapid and selective degradation of the heterochromatin adapter protein TRIM28 triggers dissociation of transcriptional condensates from loci encoding super-enhancer (SE)-driven pluripotency genes and their association with transcribed ERV loci in murine embryonic stem cells. Knockdown of ERV RNAs or forced expression of SE-enriched transcription factors rescued condensate localization at SEs in TRIM28-degraded cells. In a biochemical reconstitution system, ERV RNA facilitated partitioning of RNA polymerase II and the Mediator coactivator into phase-separated droplets. In TRIM28 knockout mouse embryos, single-cell RNA-seq analysis revealed specific depletion of pluripotent lineages. We propose that coding and noncoding nascent RNAs, including those produced by retrotransposons, may facilitate 'hijacking' of transcriptional condensates in various developmental and disease contexts.
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