Mitotic retention of H3K27 acetylation promotes rapid topological and transcriptional resetting of stem cell-related genes and enhancers upon G1 entry

BioRxiv : the Preprint Server for Biology
B. Pelham-WebbEffie Apostolou


The identity of dividing cells is challenged during mitosis, as transcription is halted and chromatin architecture drastically altered. How cell type-specific gene expression and genomic organization are faithfully reset upon G1 entry in daughter cells remains elusive. To address this issue, we characterized at a genome-wide scale the dynamic transcriptional and architectural resetting of mouse pluripotent stem cells (PSCs) upon mitotic exit. This revealed distinct patterns of transcriptional reactivation with rapid induction of stem cell genes and their enhancers, a more gradual recovery of metabolic and cell cycle genes, and a weak and transient activation of lineage-specific genes only during G1. Topological reorganization also occurred in an asynchronous manner and associated with the levels and kinetics of transcriptional reactivation. Chromatin interactions around active promoters and enhancers, and particularly super enhancers, reformed at a faster rate than CTCF/Cohesin-bound structural loops. Interestingly, regions with mitotic retention of the active histone mark H3K27ac and/or specific DNA binding factors showed faster transcriptional and architectural resetting, and chemical inhibition of H3K27 acetylation specifica...Continue Reading

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