Fig. 4: Transcriptional control involving enhancer–promoter interactions.
From: Enhancer–promoter specificity in gene transcription: molecular mechanisms and disease associations
a Gene expression occurs in a discontinuous fashion, referred to as bursting. Enhancers can increase bursting frequency to augment cognate gene expression via increased enhancer–promoter contact. Enhancer bursting, unlike promoter bursting, and synchronization of enhancer/promoter activation have yet to be visualized by imaging techniques. b Interaction of IDR-containing proteins (TFs, cofactors, and other chromatin-associated proteins) and their association with eRNAs results in formation of biocondensates. These phase-separated structures are thought to form at specific genomic loci to facilitate robust transcriptional activation. c Multiple mechanisms may allow enhancers to induce pause release at promoters by discharging pausing factors. Anti-pause enhancers (A-PEs) increase gene expression from cognate promoters via JMJD6-dependent dismissal of 7SK snRNA and HEXIM1/2. Alternatively, eRNAs can cause disassociation of promoter-bound NELF.
