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. 2012 May;86(10):5926–5930. doi: 10.1128/JVI.06384-11

Fig 1.

Fig 1

The G3A/C8U mutation results in a significant increase in influenza virus minireplicon driven gene expression. (A) Depiction of the corkscrew structure adopted by wild-type influenza A viral segments (left panel) and the two mutations introduced in the promoter (right panel). These mutations result in a vRNA promoter that more closely resembles the cRNA promoter (note the base pairs that form the stem of the 5′ end of the vRNA molecule). (B) Minireplicon assays were performed in order to determine the effect of the G3A/C8U double mutation on reporter gene expression. WT-LUC, the reporter gene flanked by the wild-type noncoding sequences. G3A/C8U-LUC, the reporter gene flanked by the mutated noncoding sequences. As a negative control, the plasmid encoding the viral NP protein was omitted (vPOL-NP). The experiment was repeated four times. Error bars represent standard errors.