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TRIM33 switches off Ifnb1 gene transcription during the late phase of macrophage activation
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Journal Article
TRIM33 switches off Ifnb1 gene transcription during the late phase of macrophage activation
2015
Overview
Despite its importance during viral or bacterial infections, transcriptional regulation of the interferon-β gene (
Ifnb1
) in activated macrophages is only partially understood. Here we report that TRIM33 deficiency results in high, sustained expression of
Ifnb1
at late stages of toll-like receptor-mediated activation in macrophages but not in fibroblasts. In macrophages, TRIM33 is recruited by PU.1 to a conserved region, the
Ifnb1
Control Element (ICE), located 15 kb upstream of the
Ifnb1
transcription start site. ICE constitutively interacts with
Ifnb1
through a TRIM33-independent chromatin loop. At late phases of lipopolysaccharide activation of macrophages, TRIM33 is bound to ICE, regulates
Ifnb1
enhanceosome loading, controls
Ifnb1
chromatin structure and represses
Ifnb1
gene transcription by preventing recruitment of CBP/p300. These results characterize a previously unknown mechanism of macrophage-specific regulation of
Ifnb1
transcription whereby TRIM33 is critical for
Ifnb1
gene transcription shutdown.
Transcriptional regulation of the interferon-β gene (
Ifnb1
) in macrophages is a critical immune event. Here, Ferri
et al
. show that, at late phases of macrophages activation, TRIM33 bound to a distal repressor element suppresses
Ifnb1
transcription by preventing recruitment of CBP/p300.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Pub. Group
Subject
