Histone post-translational modifications articles from across Nature Portfolio

The mechanisms of stalled fork degradation in BRCA1/2-deficient cells remain unclear. UFL1, an UFM1-specific E3 ligase, was found to catalyze PTIP UFMylation at lysine 148, promoting stalled fork degradation by the MRE11 nuclease.

Hu et al. describe how histone H1.0 regulates myofibroblast activation, linking force generation to nuclear organization and gene transcription.

Cryo-EM studies reveal that RYBP–PRC1 uses two distinct interfaces for binding unmodified and H2Aub1-modified nucleosomes. These binding modes enable the complex to generate H2Aub1 chromatin domains by a read–write mechanism.

The structure of the nucleosome-bound human Bre1 complex reveals that its two RING domains bind the acidic patch and nucleosomal DNA, directing the E2 enzyme and ubiquitin for H2BK120-specific ubiquitination. The binding mode suggests a possible regulatory mechanism through nucleosomal DNA flexibility.

Combination of BET inhibitors (BETi) with immunotherapy has been reported to be synergic for the treatment of non-small cell lung carcinoma (NSCLC). Here, the authors show that BETi-induced epigenetic reprogramming downregulates the expression of NK cell inhibitory receptors on NK cells, increasing their activation and cytotoxicity against NSCLC.

Trypanosoma brucei DOT1A and DOT1B methylate H3K76 without H2B-ubiquitin. Based on structural and enzymatic data, Frisbie et al. reveal a mechanism of how these enzymes cooperatively and efficiently tri-methylate H3K76 in a ubiquitin-independent way.

The microbiome is implicated in a study that involves the metabolism of dietary fibre into short-chain fatty acids, which provides a biochemical link to the poorly understood histone butyrylation.

We developed MAbID, a method for combined genomic profiling of histone modifications and chromatin-binding proteins in single cells, enabling researchers to study the interconnectivity between gene-regulatory mechanisms. We demonstrated MAbID’s implementation in profiling multifactorial changes in chromatin signatures during in vitro neural differentiation and in primary mouse bone marrow tissue.

Martin et al. report that the EP400/TIP60 complex can compensate for function of the SWI/SNF complex to remodel chromatin at some promoters.

The development of an epigenetics-focused, CRISPR-based high-content functional genomics screening platform provides insight into chromatin regulation and uncovers a potential strategy to treat an aggressive type of leukemia.

Bulut-Karslıoğlu remembers the publication of two seminal papers that described bivalent chromatin and how this discovery continues to affect research to this day.