Alternative splicing, a new target to block cellular gene expression by poliovirus 2A protease

Biochem Biophys Res Commun. 2011 Oct 14;414(1):142-7. doi: 10.1016/j.bbrc.2011.09.040. Epub 2011 Sep 16.

Abstract

Viruses have developed multiple strategies to interfere with the gene expression of host cells at different stages to ensure their own survival. Here we report a new role for poliovirus 2A(pro) modulating the alternative splicing of pre-mRNAs. Expression of 2A(pro) potently inhibits splicing of reporter genes in HeLa cells. Low amounts of 2A(pro) abrogate Fas exon 6 skipping, whereas higher levels of protease fully abolish Fas and FGFR2 splicing. In vitro splicing of MINX mRNA using nuclear extracts is also strongly inhibited by 2A(pro), leading to accumulation of the first exon and the lariat product containing the unspliced second exon. These findings reveal that the mechanism of action of 2A(pro) on splicing is to selectively block the second catalytic step.

MeSH terms

  • Alternative Splicing*
  • Cysteine Endopeptidases / genetics
  • Cysteine Endopeptidases / metabolism*
  • Exons
  • Gene Expression*
  • Genes, Reporter
  • HeLa Cells
  • Humans
  • Poliomyelitis / genetics
  • Receptor, Fibroblast Growth Factor, Type 2 / genetics
  • Viral Proteins / genetics
  • Viral Proteins / metabolism*
  • fas Receptor / genetics

Substances

  • Viral Proteins
  • fas Receptor
  • FGFR2 protein, human
  • Receptor, Fibroblast Growth Factor, Type 2
  • Cysteine Endopeptidases
  • picornain 2A, Picornavirus