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

Darya A. Haas, Arno Meiler, Katharina Geiger, Carola Vogt, Ellen Preuss, Georg Kochs, Andreas Pichlmair

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 novorecruitment 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 novorecruitment 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.

Bioruptor Plus

Share this article

April, 2018


Products used in this publication

  • Bioruptor Plus Sonication Device
    Bioruptor® Plus sonication device


  • CNET 2022
    Gif-Sur-Yvette, France
    Jul 4-Jul 6, 2022
 See all events


 See all news

The European Regional Development Fund and Wallonia are investing in your future.

Extension of industrial buildings and new laboratories.

       Site map   |   Contact us   |   Conditions of sales   |   Conditions of purchase   |   Privacy policy   |   Diagenode Diagnostics