Extended Data Fig. 10: A-to-I editing analysis of mRNA in mouse and human ADAR1 Zα domain mutant cells.

a, Primary lung fibroblasts derived from mice of the indicated genotypes were stimulated for 16 h with 200 U/mL IFN-α or left untreated. The total number of mouse repeat elements that underwent A-to-I editing was determined for 3 independent cell lines per genotype. Lines represent the mean. b, Boxplot illustrating the distribution of repeat elements in which editing activity was observed in 3 individual cell lines per genotype treated or not with IFN-α as indicated in (a). c, Venn diagrams displaying the number of repeat elements of which A-to-I editing activity was restricted to a single genotype (Adar^+/- Mavs^-/- or Adar^Zα/- Mavs^-/-) or those that were detected in both groups without stimulation or following IFN-α treatment as indicated in (a). d, Graphical representation of the differential A-to-I editing profile of ADAR^Par/WT and ADAR^Zαmut HEK293 cells detected on the indicated AluSp element in Fig. 4c and its nearest inverted repeat element (AluSx1). Data points show mean + SD; P values by Welch’s t-test. e,f, The RNAfold webtool was used to predict the folding structure and minimum free energy (MFE) of dsRNA formed by the AluSp:AluSx1 hybrid in complete absence of A-to-I editing (e) and when fully edited (f) at the A-to-I sites identified in (d). The A-to-I editing sites are indicated with black arrows. g, Transfection of HT-29 ZBP1^WT with 50 ng of BPNT1 3’UTR duplex RNA in combination with 3 µM GSK’840 and/or 20 µM zVAD-fmk. Cell death was analysed as in Fig. 3d. Fitted lines represent a logistic growth fit. Data points show the mean of 2 technical replicates + SD and are representative of 3 independent experiments

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