Modification of enhancer chromatin: what, how and why?

By Eliezer Calo, J. Wysocka. Molecules and Cells, 2013

1,395 citations recorded by the source corpus.

Emergence of form and function during embryogenesis arises in large part through cell type- and cell state- specific variation in gene expression patterns, mediated by specialized cis-regulatory elements called enhancers. Recent large-scale epigenomic mapping revealed unexpected complexity and dynamics of enhancer utilization patterns, with 400,000 putative human enhancers annotated by the ENCODE project alone. These large-scale efforts were largely enabled through understanding that enhancers share certain stereotypical chromatin features. However, an important question still lingers: What is the functional significance of enhancer chromatin modification? Here we give an overview of enhancer-associated modifications of histones and DNA, and discuss enzymatic activities involved in their dynamic deposition and removal. We describe potential downstream effectors of these marks and propose models for exploring functions of chromatin modification in regulating enhancer activity during development.

Subfields: Molecular Biology, Plant Science

View Paper: https://www.semanticscholar.org/paper/0863c349f45a85c6b8fe9c340e76f10c400a0d26

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Citations in the corpus

PEDLA: predicting enhancers with a deep learning-based algorithmic framework (2016, methodology): “(3) Use the Viterbi algorithm to predict the final state of unlabelled data based on the triple (π, A, B).”
Integrated single-cell analysis maps the continuous regulatory landscape of human hematopoietic differentiation (2018, background): “The shape of this landscape is largely defined by transcription factors (‘‘guy-wires’’), which recruit chromatin effectors to reconfigure chromatin (Calo and Wysocka, 2013; Long et al., 2016) and promote new cellular phenotypes (Graf and Enver, 2009; Takahashi and Yamanaka, 2006).”
A Comparative Encyclopedia of DNA Elements in the Mouse Genome (2014, methodology): “Instead of gene expression levels, we selected the histone modification H3K27ac as an indicator of promoter or enhancer activity as previously reported 49 .”
Super-enhancers in the control of cell identity and disease. (2013, positive): “Previous studies have described the activities of RNA polymerase II and various cofactors, chromatin regulators and RNA at specific enhancers (Calo and Wysocka, 2013; Kagey et al., 2010; Lai et al., 2013; Lam et al., 2013; Li et al., 2013; Ling et al., 2004; Mousavi et al., 2013; Natoli and Andrau, ”
Transcriptional enhancers: from properties to genome-wide predictions (2014, neutral): “100 ).”
A double take on bivalent promoters. (2013, background): “…in ES cells have revealed the presence of distinct histone marks at certain genomic domains, such as H3K4me1 and acetylation of H3K27 (H3K27ac) within active enhancers as well as H3K4me3 and H3K27me3 within active and repressed promoters, respectively (Zhou et al. 2011; Calo and Wysocka 2013).”
Analysis of nascent RNA identifies a unified architecture of initiation regions at mammalian promoters and enhancers (2014, neutral): “Alternatively, permissive chromatin could arise concomitantly with transcription factor binding and transcription 14 .”
The mechanisms behind the therapeutic activity of BET bromodomain inhibition (2014, background): “S cells and subsequently in Ly1 lymphoma cells (Chapuy et al., 2013; Lovén et al., 2013).”