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

Haas, D. A., Meiler, A., Geiger, K., Vogt, C., Preuss, E., Kochs, G., et al. (2018). Viral targeting of TFIIB impairs de novo polymerase II recruitment and affects antiviral immunity. PLoS Pathogens, 14(4): e1006980. doi:10.1371/journal.ppat.1006980.

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journal.ppat.1006980.pdf (Publisher version), 18MB
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journal.ppat.1006980.pdf
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Data Availability: All relevant data are within the paper and its Supporting Information files. All transcriptome analysis files are available from the GEO database (accession numbers GSE105152, GSE105153).
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© 2018 Haas et al.

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 Creators:
Haas, Darya A.1, Author              
Meiler, Arno1, Author              
Geiger, Katharina2, Author
Vogt, Carola2, Author
Preuss, Ellen2, Author
Kochs, Georg2, Author
Pichlmair, Andreas1, Author              
Affiliations:
1Pichlmair, Andreas / Innate Immunity, Max Planck Institute of Biochemistry, Max Planck Society, ou_1565166              
2external, ou_persistent22              

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Free keywords: TRANSCRIPTION FACTOR IIB; INTERFERON REGULATORY FACTOR-3; THOGOTO-VIRUS SEGMENT-6; PRE-INITIATION COMPLEX; TATA-BINDING PROTEIN; NF-KAPPA-B; RNA-POLYMERASE; IN-VIVO; PAUSE RELEASE; HUMAN-CELLSMicrobiology; Parasitology; Virology;
 Abstract: 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.

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Language(s): eng - English
 Dates: 2018
 Publication Status: Published online
 Pages: 27
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Degree: -

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Project name : ERC StG 311339/iVIP
Grant ID : -
Funding program : ERC
Funding organization : -
Project name : Grants (PI 1084 3/-1) and TRR179
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Funding program : -
Funding organization : Deutsche Forschungsgemeinschaft (DFG)

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Title: PLoS Pathogens
  Other : PLoS Pathog.
Source Genre: Journal
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Publ. Info: San Francisco, CA : Public Library of Science
Pages: - Volume / Issue: 14 (4) Sequence Number: e1006980 Start / End Page: - Identifier: ISSN: 1553-7366
CoNE: https://pure.mpg.de/cone/journals/resource/1000000000018830