Leading science, pioneering therapies
CRM Publications

Transcription-coupled deposition of histone modifications during MHC class II gene activation.

TitleTranscription-coupled deposition of histone modifications during MHC class II gene activation.
Publication TypeJournal Article
Year of Publication2007
AuthorsRybtsova N, Leimgruber E, Seguín-Estévez Q, Dunand-Sauthier I, Krawczyk M, Reith W
JournalNucleic Acids Res
Volume35
Issue10
Pagination3431-41
Date Published2007
ISSN1362-4962
Keywords5' Flanking Region, Acetylation, Cell Line, Genes, MHC Class II, Histones, HLA-DR alpha-Chains, HLA-DR Antigens, Humans, Interferon-gamma, Kinetics, Methylation, Protein Processing, Post-Translational, Transcriptional Activation
Abstract

Posttranslational histone modifications associated with actively expressed genes are generally believed to be introduced primarily by histone-modifying enzymes that are recruited by transcription factors or their associated co-activators. We have performed a comprehensive spatial and temporal analyses of the histone modifications that are deposited upon activation of the MHC class II gene HLA-DRA by the co-activator CIITA. We find that transcription-associated histone modifications are introduced during two sequential phases. The first phase precedes transcription initiation and is characterized exclusively by a rapid increase in histone H4 acetylation over a large upstream domain. All other modifications examined, including the acetylation and methylation of several residues in histone H3, are restricted to short regions situated at or within the 5' end of the gene and are established during a second phase that is concomitant with ongoing transcription. This second phase is completely abrogated when elongation by RNA polymerase II is blocked. These results provide strong evidence that transcription elongation can play a decisive role in the deposition of histone modification patterns associated with inducible gene activation.

DOI10.1093/nar/gkm214
Alternate JournalNucleic Acids Res.
PubMed ID17478518
PubMed Central IDPMC1904273
Publication institute
Other