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Viral targeting of TFIIB impairs de novo polymerase II recruitment and affects antiviral immunity

ABSTRACT: Viral targeting of TFIIB impairs de novo polymerase II recruitment and affects antiviral immunity

PROVIDER: PRJNA414967 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6189790.fastq.gz	Fastqsanger.gz
	SRR6189800.fastq.gz	Fastqsanger.gz
	SRR6189781.fastq.gz	Fastqsanger.gz
	SRR6189791.fastq.gz	Fastqsanger.gz
	SRR6189801.fastq.gz	Fastqsanger.gz

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Viral targeting of TFIIB impairs de novo polymerase II recruitment and affects antiviral immunity.

Project description:Viruses have evolved a plethora of mechanisms to target host antiviral responses. Here, we propose a yet uncharacterized mechanism of immune regulation by the orthomyxovirus Thogoto virus (THOV) ML protein through engaging general transcription factor TFIIB. ML generates a TFIIB depleted nuclear environment by re-localizing it into the cytoplasm. Although a broad effect on gene expression would be anticipated, ML expression, delivery of an ML-derived functional domain or experimental depletion of TFIIB only leads to altered expression of a limited number of genes. Our data indicate that TFIIB is critically important for the de novo recruitment of Pol II to promoter start sites and that TFIIB may not be required for regulated gene expression from paused promoters. Since many immune genes require de novo recruitment of Pol II, targeting of TFIIB by THOV represents a neat mechanism to affect immune responses while keeping other cellular transcriptional activities intact. Thus, interference with TFIIB activity may be a favourable site for therapeutic intervention to control undesirable inflammation.

| S-EPMC5927403 | biostudies-literature

Viral targeting of TFIIB impairs de novo polymerase II recruitment and affects antiviral immunity

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-04-01 | GSE105154 | GEO

TFIIB

Project description:TFIIB

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Genome wide TFIIB binding during postnatal and pressure-induced cardiac hypertrophy

Project description:Purpose: To identify the differential TFIIB bindingl patterns during postnatal cardiac growth, pressure-induced cardiac hypertrophy and adult mouse hearts Methods: Hearts were extracted from 1-2day old C57 mice, from mice subjecetd to Transaortic coarctation or adult mice. The hearts were sent to Active Motif for TFIIB- ChIP-Seq. Results: In accordance with previosly published data (Sayed D, et. al. JBC, 2013 Jan 25;288(4):2546-58) with genome wide polII and H3K9ac status during cardiac hypertrophy (GSE50637), Denovo TFIIB recruitment was restricted to speclaized genes with cardiac hypertrophy. Hearts were extracted from 1-2day old C57 mice, from mice subjecetd to Transaortic coarctation or adult mice. The hearts were sent to Active Motif for TFIIB- ChIP-Seq.

2014-11-17 | E-GEOD-56813 | biostudies-arrayexpress

Genome wide TFIIB binding during postnatal and pressure-induced cardiac hypertrophy

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Transcriptomic effects of caspase cleavage at TFIIB residue D207 during apoptosis and KSHV infection [TFIIB(D207A)]

Project description:Cellular stressors often cause widespread repression of RNA polymerase II (RNAP II) activity, which is thought to facilitate a focused transcriptional output towards stress resolution. In many cases, however, the underlying regulatory mechanisms remain unknown. Here, we demonstrate that stress-induced downregulation of the general transcription factor TFIIB tempers expression of specific stimulus response genes. Following a variety of stressors, TFIIB is proteolytically cleaved between its cyclin folds at conserved aspartic acid residue D207 by caspases- 3 and 7. Cleavage in this portion of the protein significantly reduces the ability of TFIIB to form a TBP-TFIIB-DNA promoter complex in vitro. Using both overexpression and endogenous base-editing, we find that B and T cells that are unable to cleave TFIIB upregulate expression of a select gene set during apoptosis. These TFIIB-sensitive genes are primarily short, stimulus-responsive and proto-oncogenic loci, and cleavage of TFIIB temporally restricts their expression. Failure to cleave TFIIB during stress leads to aberrant lymphocyte proliferation during chemical perturbation. Hence, caspase targeting of TFIIB destabilizes transcription to tune gene expression, allowing for proper stress resolution.

2026-02-01 | GSE250393 | GEO

Deregulated immune cell recruitment impairs human diabetic wound healing

Project description:Deregulated immune cell recruitment impairs human diabetic wound healing

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CTD tyrosine phosphorylation impairs termination factor recruitment to transcribing RNA polymerase II

Project description:ChIP-chip was performed to identify the genomic binding locations for the termination factors Nrd1, and Rtt103, and for RNA polymerase (Pol) II phosphorylated at the tyrosine 1 and threonine 4 position of its C-terminal domain (CTD). In different phases of the transcription cycle, Pol II recruits different factors via its CTD, which consists of heptapeptide repeats with the sequence Tyr1-Ser2-Pro3-Thr4-Ser5-Pro6-Ser7. Here we show that the CTD of transcribing yeast Pol II is phosphorylated at Tyr1, and that this impairs recruitment of termination factors. Tyr1 phosphorylation levels rise downstream of the transcription start site (TSS), and decrease before the polyadenylation (pA) site. Tyr1-phosphorylated gene bodies are depleted of CTD-binding termination factors Nrd1, Pcf11, and Rtt103. Tyr1 phosphorylation blocks CTD binding by these termination factors, but stimulates binding of elongation factor Spt6. These results show that CTD modifications can not only stimulate but also block factor recruitment, and lead to an extended CTD code for transcription cycle coordination.

2012-06-29 | E-MTAB-1060 | biostudies-arrayexpress

Gene knockdown suggests a new paradigm for transcription factor TFIIB functionality

Project description:Experimental and bioinformatic studies of transcription initiation by RNA polymerase II (RNAP2) have revealed a mechanism of RNAP2 transcription initiation less uniform across gene promoters than initially thought. However, the general transcription factor TFIIB is presumed to be universally required for RNAP2 transcription initiation. Based on bioinformatic analysis of data, TFIIB knockdown in primary and transformed cell lines, and in vitro transcription experiments, we report that TFIIB is dispensable for transcription of most human promoters, but is essential for HSV-1 gene transcription and replication. We report a novel cell cycle TFIIB regulation and involvement of the acetylated TFIIB variant in chromosomal condensation. Taken together, these results establish a new paradigm for TFIIB functionality as a determinant of the human transcriptome, which when downregulated has potent anti-viral effects.

2014-12-31 | GSE48847 | GEO