A new paradigm for transcription factor TFIIB functionality

Sci Rep. 2014 Jan 20:4:3664. 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylation
  • Animals
  • Binding Sites
  • Cell Cycle / genetics
  • Cell Line
  • Datasets as Topic
  • Gene Expression
  • Gene Expression Profiling
  • Gene Expression Regulation
  • Gene Expression Regulation, Viral
  • Gene Knockdown Techniques
  • Gene Silencing
  • Genes, Lethal
  • Genome, Human
  • Herpesvirus 1, Human / genetics
  • Humans
  • Organ Specificity / genetics
  • Protein Binding
  • RNA Polymerase II / chemistry
  • RNA Polymerase II / metabolism
  • Transcription Factor TFIIB / deficiency
  • Transcription Factor TFIIB / genetics
  • Transcription Factor TFIIB / metabolism*
  • Transcription Initiation Site
  • Transcription, Genetic
  • Transcriptome

Substances

  • Transcription Factor TFIIB
  • RNA Polymerase II