Human MAF1 targets and represses active RNA polymerase III genes by preventing recruitment rather than inducing long-term transcriptional arrest.

Détails

Ressource 1Télécharger: 624 (1).pdf (5009.52 [Ko])
Etat: Serval
Version: Final published version
ID Serval
serval:BIB_9C3459E28377
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Human MAF1 targets and represses active RNA polymerase III genes by preventing recruitment rather than inducing long-term transcriptional arrest.
Périodique
Genome research
Auteur(s)
Orioli A., Praz V., Lhôte P., Hernandez N.
ISSN
1549-5469 (Electronic)
ISSN-L
1088-9051
Statut éditorial
Publié
Date de publication
03/2016
Peer-reviewed
Oui
Volume
26
Numéro
5
Pages
624-635
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: ppublish
Résumé
RNA polymerase III (Pol III) is tightly controlled in response to environmental cues, yet a genomic-scale picture of Pol III regulation and the role played by its repressor MAF1 is lacking. Here, we describe genome-wide studies in human fibroblasts that reveal a dynamic and gene-specific adaptation of Pol III recruitment to extracellular signals in an mTORC1-dependent manner. Repression of Pol III recruitment and transcription are tightly linked to MAF1, which selectively localizes at Pol III loci, even under serum-replete conditions, and increasingly targets transcribing Pol III in response to serum starvation. Combining Pol III binding profiles with EU-labeling and high-throughput sequencing of newly synthesized small RNAs, we show that Pol III occupancy closely reflects ongoing transcription. Our results exclude the long-term, unproductive arrest of Pol III on the DNA as a major regulatory mechanism and identify previously uncharacterized, differential coordination in Pol III binding and transcription under different growth conditions.

Mots-clé
Cell Line, Humans, Multiprotein Complexes/genetics, Multiprotein Complexes/metabolism, RNA Polymerase III/genetics, RNA Polymerase III/metabolism, Repressor Proteins/genetics, Repressor Proteins/metabolism, TOR Serine-Threonine Kinases/genetics, TOR Serine-Threonine Kinases/metabolism, Transcription, Genetic/physiology
Pubmed
Open Access
Oui
Création de la notice
15/03/2016 20:46
Dernière modification de la notice
08/05/2019 22:40
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