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Chromatin

BRD4 kicks out nucleosomes with its HAT

Nature Reviews Molecular Cell Biology volume 17, pages 396–397 (2016)Cite this article

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Chromatin decompaction following mitosis is crucial for reactivating transcription, and histone acetylation is an important regulator of this process. It is known that overexpression of BRD4 correlates with chromatin decompaction and transcriptional reactivation, indicating that it might regulate histone acetylation, possibly by acting as a HAT. Indeed, Devaiah et al. found that recombinant mouse BRD4 acetylated histones as well as nucleosomes in vitro and when expressed in human and mouse cell lines. Notably, BDR4 acetylated amino-terminal tails of histones (which are canonical substrates of HATs), as well as Lys122 of histone H3 (H3K122ac), which resides at the histone–DNA interface. Consistent with this observation, expression of BRD4 in cells increased H3K122ac levels, and this was dependent on its HAT activity.

To investigate the importance of BRD4-mediated H3K122 acetylation in vivo, the authors knocked out BRD4 in the developing thymus, which markedly decreased H3K122ac levels and interfered with cell differentiation in this organ. Similarly, BRD4 deficiency impaired H3K122 acetylation in mouse embryonic fibroblasts and compromised their viability.

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References

  1. Devaiah, B. N. et al. BRD4 is a histone acetyltransferase that evicts nucleosomes from chromatin. Nat. Struct. Mol. Biol. http://dx.doi.org/10.1038/nsmb.3228 (2016)

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  1. Paulina Strzyz
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Strzyz, P. BRD4 kicks out nucleosomes with its HAT. Nat Rev Mol Cell Biol 17, 396–397 (2016). https://doi.org/10.1038/nrm.2016.72

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