A new paradigm for transcription factor TFIIB functionality

Sci Rep. 2014 Jan 20;4:3664. doi: 10.1038/srep03664.

Vladimir Gelev ¹, Janice M Zabolotny ¹, Martin Lange ², Makoto Hiromura ², Sang Wook Yoo ², Joseph S Orlando ³, Anna Kushnir ³, Nobuo Horikoshi ², Eric Paquet ⁴, Dimcho Bachvarov ⁴, Priscilla A Schaffer ³, Anny Usheva ²

Affiliations

1 1] Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA [2].
2 Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
3 Department of Microbiology and Molecular Genetics, Program in Virology, Harvard Medical School at Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.
4 Centre Hospitalier Universitaire de Québec (CHUQ)-Centre de Recherche, Hopital L'Hôtel-Dieu de Québec et Université Laval, Québec G1R 2J6, Canada.

PMID: 24441171 DOI: 10.1038/srep03664

Abstract

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 and effects of TFIIB knockdown in primary and transformed cell lines on cellular functionality and global gene expression, we report that TFIIB is dispensable for transcription of many human promoters, but is essential for herpes simplex virus-1 (HSV-1) gene transcription and replication. We report a novel cell cycle TFIIB regulation and localization of the acetylated TFIIB variant on the transcriptionally silent mitotic chromatids. Taken together, these results establish a new paradigm for TFIIB functionality in human gene expression, which when downregulated has potent anti-viral effects.

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