scholarly journals First Exon Length Controls Active Chromatin Signatures and Transcription

Cell Reports ◽  
2012 ◽  
Vol 2 (1) ◽  
pp. 62-68 ◽  
Author(s):  
Nicole I. Bieberstein ◽  
Fernando Carrillo Oesterreich ◽  
Korinna Straube ◽  
Karla M. Neugebauer
Keyword(s):  
Active Chromatin ◽  
Exon Length

scholarly journals Site-specific ubiquitylation acts as a regulator of linker histone H1

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Eva Höllmüller ◽  
Simon Geigges ◽  
Marie L. Niedermeier ◽  
Kai-Michael Kammer ◽  
Simon M. Kienle ◽  
...  
Keyword(s):  
Posttranslational Modifications ◽  
Histone H1 ◽  
Linker Histone ◽  
Active Chromatin ◽  
Site Specific ◽  
Linker Histone H1 ◽  
Fundamental Process ◽  
Core Histones ◽  
Wide Scale

AbstractDecoding the role of histone posttranslational modifications (PTMs) is key to understand the fundamental process of epigenetic regulation. This is well studied for PTMs of core histones but not for linker histone H1 in general and its ubiquitylation in particular due to a lack of proper tools. Here, we report on the chemical synthesis of site-specifically mono-ubiquitylated H1.2 and identify its ubiquitin-dependent interactome on a proteome-wide scale. We show that site-specific ubiquitylation of H1 at position K64 modulates interactions with deubiquitylating enzymes and the deacetylase SIRT1. Moreover, it affects H1-dependent chromatosome assembly and phase separation resulting in a more open chromatosome conformation generally associated with a transcriptionally active chromatin state. In summary, we propose that site-specific ubiquitylation plays a general regulatory role for linker histone H1.

scholarly journals ChIP-seq profiling of the active chromatin marker H3K4me3 and PPARγ, CEBPα and LXR target genes in human SGBS adipocytes

Genomics Data ◽  
2014 ◽  
Vol 2 ◽  
pp. 230-236 ◽  
Author(s):  
Mafalda Galhardo ◽  
Lasse Sinkkonen ◽  
Philipp Berninger ◽  
Jake Lin ◽  
Thomas Sauter ◽  
...  
Keyword(s):  
Target Genes ◽  
Active Chromatin

scholarly journals Epigenomic landscape of human colorectal cancer unveils an aberrant core of pan-cancer enhancers orchestrated by YAP/TAZ

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Giulia Della Chiara ◽  
Federica Gervasoni ◽  
Michaela Fakiola ◽  
Chiara Godano ◽  
Claudia D’Oria ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cell ◽  
De Novo ◽  
Epigenetic Alterations ◽  
Human Colorectal Cancer ◽  
Active Chromatin ◽  
Extensive Cell Death ◽  
Extensive Cell ◽  
Pan Cancer ◽  
Tumor Maintenance

AbstractCancer is characterized by pervasive epigenetic alterations with enhancer dysfunction orchestrating the aberrant cancer transcriptional programs and transcriptional dependencies. Here, we epigenetically characterize human colorectal cancer (CRC) using de novo chromatin state discovery on a library of different patient-derived organoids. By exploring this resource, we unveil a tumor-specific deregulated enhancerome that is cancer cell-intrinsic and independent of interpatient heterogeneity. We show that the transcriptional coactivators YAP/TAZ act as key regulators of the conserved CRC gained enhancers. The same YAP/TAZ-bound enhancers display active chromatin profiles across diverse human tumors, highlighting a pan-cancer epigenetic rewiring which at single-cell level distinguishes malignant from normal cell populations. YAP/TAZ inhibition in established tumor organoids causes extensive cell death unveiling their essential role in tumor maintenance. This work indicates a common layer of YAP/TAZ-fueled enhancer reprogramming that is key for the cancer cell state and can be exploited for the development of improved therapeutic avenues.

Transcriptionally active chromatin

1983 ◽  
Vol 9 (1-2) ◽  
pp. 9-17 ◽  
Author(s):  
R. Tsanev
Keyword(s):  
Active Chromatin
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