Fig. 3: New FluPol–Pol II–DSIF elongation complex interfaces.
From: Mechanism of co-transcriptional cap snatching by influenza polymerase
a–c, Zoom-ins on the interfaces between the FluPol PA endonuclease domain and the DSIF KOWx-4 domain (a), the FluPol PB2 cap-binding domain and RPB1 (b) or RPB3 and RPB11 (c). Mutated amino acids mutated are shown in stick representation and coloured by heteroatoms if the mutation reduced FluPol activity significantly in a cell-based minigenome assay. d, Cell-based minigenome assay of A/WSN/33 FluPol activity for the indicated PA and PB2 mutants. HEK-293T cells were co-transfected with plasmids encoding PB2, PB1, PA and NP with a model vRNA encoding firefly luciferase. Luminescence was normalized to a transfection control and is represented as percentage of wild-type (WT) FluPol. The K635A mutant was used a transcription-defective control. The dotted line represents background signal as measured in the absence of the PA subunit (∆PA). Each point reflects one biological replicate (n = 3), depicted as mean ± s.d., ***P < 0.001, one-way ANOVA on log-transformed data with Dunnett′s multiple comparisons test referenced to wild-type FluPol.
