Key result
Poliovirus 2A protease induces a selective nucleo-cytoplasmic translocation of splicing factors, creating an imbalance between HuR and TIA1/TIAR that promotes Fas exon 6 skipping.
Poliovirus 2A protease regulates alternative pre-mRNA splicing by inducing the nucleo-cytoplasmic redistribution of specific splicing factors.
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May alter Fas signaling in infected cells; leaves open its role in poliovirus pathogenesis.
Poliovirus protease 2A (2A(pro)) obstructs host gene expression by reprogramming transcriptional and post-transcriptional regulatory events during infection. Here we demonstrate that expression of 2A(pro) induces a selective nucleo-cytoplasm translocation of several important RNA binding proteins and splicing factors. Subcellular fractionation studies, together with immunofluorescence microscopy revealed an asymmetric distribution of HuR and TIA1/TIAR in 2A(pro) expressing cells, which modulates splicing of the human Fas exon 6. Consistent with this result, knockdown of HuR or overexpression of TIA1/TIAR, leads to Fas exon 6 inclusion in 2A(pro)-expressing cells. Therefore, poliovirus 2A(pro) can target alternative pre-mRNA splicing by regulating protein shuttling between the nucleus and the cytoplasm.
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Álvarez et al. (2013) studied Poliovirus infection mechanism. Poliovirus 2A protease (2A pro) expression vs. Mock transfection or inactive 2AM mutant was evaluated on Alternative splicing of Fas exon 6 and subcellular distribution of splicing factors. Poliovirus 2A protease induces a selective nucleo-cytoplasmic translocation of splicing factors, creating an imbalance between HuR and TIA1/TIAR that promotes Fas exon 6 skipping.
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