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

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 env...

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Bibliographic Details
Published in:PLoS pathogens 2018-04, Vol.14 (4), p.e1006980-e1006980
Main Authors: Haas, Darya A, Meiler, Arno, Geiger, Katharina, Vogt, Carola, Preuss, Ellen, Kochs, Georg, Pichlmair, Andreas
Format: Article
Language:English
Subjects:
Biochemistry
Biology and Life Sciences
Cytoplasm
Deoxyribonucleic acid
DNA
Funding
Gene expression
Genes
Genomes
Immune response
Immune system
Immunity
Immunoregulation
Laboratories
Mammals
Promoters (Genetics)
Proteins
Proteomics
Recruitment
Research and analysis methods
Transcription factors
Transcription initiation factor TFIIB
Virology
Viruses
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Summary: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.
ISSN:1553-7374
1553-7366
1553-7374
DOI:10.1371/journal.ppat.1006980