Clues to quality of journals
Open Access Policy of Helmholtz Association 2016
CC Licencences
Publication Metrics
Home
Deutsch
New EVA Application
Advanced Search
Browse by ...
Publication overview
Statistics (last 5 years)
OA Publications
Submit Publication
Import publication from...
Report missing publication
Contact persons
Help
Text
Endnote (RIS)
BibTeX
DOI
PMC
 |
|
Open Access Gold as soon as Publ. Version/Full Text is submitted to ZB.
Dissecting the role of H3K64me3 in mouse pericentromeric heterochromatin.
Nat. Commun. 4:2233 (2013)
To ensure genome stability, pericentromeric regions are compacted in a dense heterochromatic structure through a combination of specific 'epigenetic' factors and modifications. A cascadal pathway is responsible for establishing pericentromeric chromatin involving chromatin modifiers and 'readers', such as H3K9 histone methyltransferases (Suv)39h and heterochromatin protein 1. Here we define how H3K64me3 on the lateral surface of the histone octamer integrates within the heterochromatinization cascade. Our data suggest that enrichment of H3K64me3 at pericentromeric chromatin foci is dependent on H3K9me3 but independent of a number of central factors such as heterochromatin protein 1, DNA methyltransferases and Suv4-20h histone methyltransferases. Our results support a model in which pericentromeric heterochromatin foci are formed along distinct pathways upon H3K9 trimethylation, involving H3K64me3 to potentially stabilize DNA-histone interactions, as well as sequential recruitment of repressive histone tail and DNA modifications. We hence suggest that multiple mechanisms ensure heterochromatin integrity at pericentromeres, with H3K64me3 as an important factor.
Impact Factor
Scopus SNIP
Scopus
Cited By
Cited By
Altmetric
0.000
0.000
24
Annotations
Special Publikation
Hide on homepage
Publication type
Article: Journal article
Document type
Scientific Article
Language
english
Publication Year
2013
HGF-reported in Year
2013
ISSN (print) / ISBN
2041-1723
e-ISSN
2041-1723
Journal
Nature Communications
Quellenangaben
Volume: 4,
Article Number: 2233
Publisher
Nature Publishing Group
Publishing Place
London
Reviewing status
Peer reviewed
POF-Topic(s)
30204 - Cell Programming and Repair
30203 - Molecular Targets and Therapies
30203 - Molecular Targets and Therapies
Research field(s)
Stem Cell and Neuroscience
Helmholtz Diabetes Center
Helmholtz Diabetes Center
PSP Element(s)
G-506200-001
G-502800-001
G-502800-001
PubMed ID
23903902
Erfassungsdatum
2013-12-31