PuSH - Publication Server of Helmholtz Zentrum München

Export: TXT Text RIS Endnote (RIS) BIB BibTeX
de Almeida, S.F.* ; Grosso, A.R.* ; Koch, F.* ; Fenouil, R.* ; Carvalho, S.* ; Andrade, J.* ; Levezinho, H.* ; Gut, M.* ; Eick, D. ; Gut, I.* ; Andrau, J.C.* ; Ferrier, P.* ; Carmo-Fonseca, M.*

Splicing enhances recruitment of methyltransferase HYPB/Setd2 and methylation of histone H3 Lys36.

Nat. Struct. Mol. Biol. 18, 977-984 (2011)
Publ. Version/Full Text DOI PMC
Open Access Gold
Several lines of recent evidence support a role for chromatin in splicing regulation. Here, we show that splicing can also contribute to histone modification, which implies bidirectional communication between epigenetic mechanisms and RNA processing. Genome-wide analysis of histone methylation in human cell lines and mouse primary T cells reveals that intron-containing genes are preferentially marked with histone H3 Lys36 trimethylation (H3K36me3) relative to intronless genes. In intron-containing genes, H3K36me3 marking is proportional to transcriptional activity, whereas in intronless genes, H3K36me3 is always detected at much lower levels. Furthermore, splicing inhibition impairs recruitment of H3K36 methyltransferase HYPB (also known as Setd2) and reduces H3K36me3, whereas splicing activation has the opposite effect. Moreover, the increase of H3K36me3 correlates with the length of the first intron, consistent with the view that splicing enhances H3 methylation. We propose that splicing is mechanistically coupled to recruitment of HYPB/Setd2 to elongating RNA polymerase II.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Scopus
Cited By
Altmetric
13.685
2.614
114
168
Tags
Annotations
Special Publikation
Hide on homepage

Edit extra information
Edit own tags
Private
Edit own annotation
Private
Hide on publication lists
on hompage
Mark as special
publikation
Publication type Article: Journal article
Document type Scientific Article
Keywords RNA-polymerase-II; Carboxyl-terminal domain; Transcriptional termination; Mammalian-cells; Active genes; Human genome; Chromatin; Set2; Elongation; Exons
Language english
Publication Year 2011
HGF-reported in Year 2011
ISSN (print) / ISBN 1545-9993
e-ISSN 1545-9985
Journal Nature Structural & Molecular Biology
Quellenangaben Volume: 18, Issue: 9, Pages: 977-984 Article Number: , Supplement: ,
Publisher Nature Publishing Group
Publishing Place New York, NY
Reviewing status Peer reviewed
Institute(s) Institute of Clinical Molecular Biology and Tumor Genetics (K.MOLBI)
POF-Topic(s) 30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Research field(s) Immune Response and Infection
PSP Element(s) G-501490-001
PubMed ID 21792193
DOI 10.1038/nsmb.2123
Scopus ID 80052445151
Erfassungsdatum 2011-10-13
[➜Report correction]