Extensive remodeling of DC function by rapid maturation-induced transcriptional silencing.

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Etat: Public
Version: de l'auteur
ID Serval
serval:BIB_33FC79D5A0AA
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Extensive remodeling of DC function by rapid maturation-induced transcriptional silencing.
Périodique
Nucleic Acids Research
Auteur(s)
Seguín-Estévez Q., Dunand-Sauthier I., Lemeille S., Iseli C., Ibberson M., Ioannidis V., Schmid C.D., Rousseau P., Barras E., Geinoz A., Xenarios I., Acha-Orbea H., Reith W.
ISSN
1362-4962 (Electronic)
ISSN-L
0305-1048
Statut éditorial
Publié
Date de publication
2014
Volume
42
Numéro
15
Pages
9641-9655
Langue
anglais
Résumé
The activation, or maturation, of dendritic cells (DCs) is crucial for the initiation of adaptive T-cell mediated immune responses. Research on the molecular mechanisms implicated in DC maturation has focused primarily on inducible gene-expression events promoting the acquisition of new functions, such as cytokine production and enhanced T-cell-stimulatory capacity. In contrast, mechanisms that modulate DC function by inducing widespread gene-silencing remain poorly understood. Yet the termination of key functions is known to be critical for the function of activated DCs. Genome-wide analysis of activation-induced histone deacetylation, combined with genome-wide quantification of activation-induced silencing of nascent transcription, led us to identify a novel inducible transcriptional-repression pathway that makes major contributions to the DC-maturation process. This silencing response is a rapid primary event distinct from repression mechanisms known to operate at later stages of DC maturation. The repressed genes function in pivotal processes--including antigen-presentation, extracellular signal detection, intracellular signal transduction and lipid-mediator biosynthesis--underscoring the central contribution of the silencing mechanism to rapid reshaping of DC function. Interestingly, promoters of the repressed genes exhibit a surprisingly high frequency of PU.1-occupied sites, suggesting a novel role for this lineage-specific transcription factor in marking genes poised for inducible repression.
Pubmed
Web of science
Open Access
Oui
Création de la notice
20/11/2014 10:37
Dernière modification de la notice
20/08/2019 13:20
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