Histone lactylation has been recently described as a novel histone post-translational modification linking cellular metabolism to epigenetic regulation.Given the expected relevance of this modification and current limited knowledge of its function, we generate genome-wide datasets of H3K18la distribution in various in vitro and in vivo samples, including mouse embryonic stem cells, macrophages, adipocytes, and mouse and human skeletal muscle. We compare them to profiles of well-established histone modifications and gene expression patterns. Supervised and unsupervised bioinformatics analysis shows that global H3K18la distribution resembles H3K27ac, although we also find notable differences. H3K18la marks active CpG island-containing promoters of highly expressed genes across most tissues assessed, including many housekeeping genes, and positively correlates with H3K27ac and H3K4me3 as well as with gene expression. In addition, H3K18la is enriched at active enhancers that lie in proximity to genes that are functionally important for the respective tissue.Overall, our data suggests that H3K18la is not only a marker for active promoters, but also a mark of tissue specific active enhancers. 

/pdf/h3k18-lactylation-marks-tissue-specific-active-enhancers-19oct6no.pdf

H3K18 lactylation marks tissue-specific active enhancers

Summary The contractile properties of adult myofibers are shaped by their Myosin heavy chain (MYH) isoform content. We identify by snATAC-seq a 42kb super-enhancer (SE) at the locus regrouping the fast Myh (fMyh) genes. By 4C-seq we show that active fMyh promoters interact with the SE by DNA looping, leading to the activation of a single promoter per nucleus. A rainbow mouse transgenic model of the locus including the SE recapitulates the endogenous spatio-temporal expression of adult fMyh genes. In situ deletion of the SE by CRISPR/Cas9 editing demonstrates its major role in the control of associated fMyh genes, and deletion of two fMyh genes at the locus reveals an active competition of the promoters for the shared SE. Last, by disrupting the organization of fMyh, we uncover positional heterogeneity within limb skeletal muscles that may underlie selective muscle susceptibility to damage in certain myopathies.

https://biorxiv.org/content/10.1101/2021.04.17.438406v1.full.pdf

A fast Myh super enhancer dictates adult muscle fiber phenotype through competitive interactions with the fast Myh genes

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A fast Myh super enhancer dictates adult muscle fiber phenotype through competitive interactions with the fast Myh genes