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Cooperative Transcriptional Activation of Antimicrobial Genes by STAT and NF-κB Pathways by Concerted Recruitment of the Mediator Complex.

Abstract：

:The transcriptional response to infection with the bacterium Listeria monocytogenes (Lm) requires cooperative signals of the type I interferon (IFN-I)-stimulated JAK-STAT and proinflammatory NF-κB pathways. Using ChIP-seq analysis, we define genes induced in Lm-infected macrophages through synergistic transcriptional activation by NF-κB and the IFN-I-activated transcription factor ISGF3. Using the Nos2 and IL6 genes as prime examples of this group, we show that NF-κB functions to recruit enzymes that establish histone marks of transcriptionally active genes. In addition, NF-κB regulates transcriptional elongation by employing the mediator kinase module for the recruitment of the pTEFb complex. ISGF3 has a major role in associating the core mediator with the transcription start as a prerequisite for TFIID and RNA polymerase II (Pol II) binding. Our data suggest that the functional cooperation between two major antimicrobial pathways is based on promoter priming by NF-κB and the engagement of the core mediator for Pol II binding by ISGF3.

journal_name

Cell Rep

journal_title

Cell reports

authors

Wienerroither S,Shukla P,Farlik M,Majoros A,Stych B,Vogl C,Cheon H,Stark GR,Strobl B,Müller M,Decker T

doi

10.1016/j.celrep.2015.06.021

subject

Has Abstract

pub_date

2015-07-14 00:00:00

pages

300-12

issue

2

issn

2211-1247

pii

S2211-1247(15)00619-1

journal_volume

12

pub_type

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