Histone post-translational modifications articles from across Nature Portfolio

Exogenously normalised chromatin immunoprecipitation sheds light on pangenomic regulation of histone methylation by hypoxia and its relation to changes in gene expression.

Toda et al. show that H3K14 ubiquitination stimulates Clr4 activity and, together with H3K9 methylation, stabilizes the CLRC complex on chromatin. This generates a feedback loop that drives heterochromatin spreading and epigenetic inheritance in fission yeast.

Caloric restriction (CR) extends lifespan but may impair immunity, with unclear hematopoietic stem cell (HSC) contribution. Here, the authors show that lifelong CR in male mice reduces white blood cells, shifts hematopoiesis toward myeloid cells, and preserves youthful HSC transcription via epigenetic KDR changes and increased PU.1 binding.

In animals, H3K4me1 marks enhancers. Here the authors show that in land plants H3K4me1 is recognized by a specific reader protein, which interacts with an H3K36 methyltransferase, to direct the establishment of H3K36me2 and H3K36me3.

Chemical modifications on DNA are key regulators of epigenetic function. Here, the authors develop 6-base-CUT&Tag to simultaneously profile multiple DNA and chromatin features on the same DNA fragment. This work reveals how specific DNA and histone marks colocalise at different enhancer regions.

Although inhibiting epigenetic enzymes holds strong therapeutic promise, off-target effects remain a prevailing challenge. This study instead targets an accessory reader to fine-tune the inhibitory pathway.

Decades of research in plants has established that the protein complexes that transcribe small interfering RNAs (siRNAs) are not targeted to DNA in a sequence-specific manner. Two independent studies uncover the recruitment of the key siRNA-producing protein RNA polymerase IV mediated by transcription factors to specific DNA sequences.

Transcriptional memory is a phenomenon that enables cells to memorize transient gene activation. A study now sheds light on epigenetic mechanisms conveying mitotic-heritable memory in the context of the IFNγ model.

Repair of DNA double-strand breaks requires chromatin opening; however, the mechanisms involved were unclear. This work shows that sequential histone deamidation and acetylation modifications induce chromatin decompaction by reducing positive charge at the DNA–nucleosome interface.

PRC2-dependent H3K27 methylation must be excluded from active genes to support appropriate transcriptional programs. Structures of PRC2 bound to nucleosome substrates containing histone modifications associated with active transcription explain how PRC2 is inhibited at active genes.

In this Tools of the Trade article, Andrey Tvardovskiy and Saulius Lukauskas introduce the web resource MARCS, which offers a set of visualization tools to explore chromatin regulatory circuits from either a protein- or modification-centred perspective.