PuSH - Publication Server of Helmholtz Zentrum München: Functional compensation among HMGN variants modulates the DNase I hypersensitive sites at enhancers.

Information

Clues to quality of journals

Open Access Policy of Helmholtz Association 2016

CC Licencences

Publication Metrics

Navigation

Home

Deutsch

Research

Advanced Search

Browse by ...

... HMGU-Authors/Consortia

... Organizational Structure

... Journal

... Publication Type

... Research Data

... Arbeitsgruppen

... Publication Year

Publication overview

Statistics

Statistics (last 5 years)

OA Publications

Publish

Submit Publication

Import publication from...

...EVA

Report missing publication

Highlights

Support & Contact

Contact persons

Help

Data protection

Helmholtz Open Science

JANE Journal Estimator

SHERPA/RoMEO

DOAJ

Export:

Text

Endnote (RIS) BIB

BibTeX

Deng, T.* ; Zhu, Z.I.* ; Zhang, S.* ; Postnikov, Y.* ; Huang, D.* ; Horsch, M. ; Furusawa, T.* ; Beckers, J. ; Rozman, J. ; Klingenspor, M. ; Amarie, O.V. ; Graw, J. ; Rathkolb, B. ; Wolf, E.* ; Adler, T. ; Busch, D.H.* ; Gailus-Durner, V. ; Fuchs, H. ; Hrabě de Angelis, M. ; van der Velde, A.* ; Tessarollo, L.* ; Ovcherenko, I.* ; Landsman, D.* ; Bustin, M.*

Functional compensation among HMGN variants modulates the DNase I hypersensitive sites at enhancers.

Genome Res. 25, 1295-1308 (2015)

Postprint

DOI

PMC

Abstract
Metrics
Extra information

DNase I hypersensitive sites (DHSs) are a hallmark of chromatin regions containing regulatory DNA such as enhancers and promoters; however, the factors affecting the establishment and maintenance of these sites are not fully understood. We now show that HMGN1 and HMGN2, nucleosome-binding proteins that are ubiquitously expressed in vertebrate cells, maintain the DHSs landscape of mouse embryonic fibroblasts (MEFs) synergistically. Loss of one of these HMGN variants led to a compensatory increase of binding of the remaining variant. Genome wide mapping of the DHSs in Hmgn1-/-, Hmgn2-/- and Hmgn1-/-n2-/- MEFs reveals that loss of both, but not a single HMGN variant, leads to significant remodeling of the DHSs landscape, especially at enhancer regions marked by H3K4me1 and H3K27ac. Loss of HMGN variants affects the induced expression of stress responsive genes in MEFs, the transcription profiles of several mouse tissues, and leads to altered phenotypes that are not seen in mice lacking only one variant. We conclude that the compensatory binding of HMGN variants to chromatin maintains the DHSs landscape and the transcription fidelity and is necessary to retain wild type phenotypes. Our study provides insights into mechanisms that maintain regulatory sites in chromatin and into functional compensation among nucleosome binding architectural proteins.

Impact Factor

Scopus SNIP

Web of Science
Times Cited

Scopus
Cited By

Altmetric

14.630

2.916