Fig. 3
From: The majority of A-to-I RNA editing is not required for mammalian homeostasis
ADAR2 loss does not modify the transcriptional signature associated with the loss of Adar1-mediated RNA editing. Analysis of differential gene expression from 12-week-old male brains of a Adar1+/+Ifih1−/− (WT) compared to Adar1E861A/E861AIfih1−/− (E861A); b Adar1+/+Ifih1−/−Adarb1−/−Gria2R/R (ADAR2 null) compared to Adar1E861A/+Ifih1−/−Adarb1+/−Gria2R/R (dHet); c Adar1E861A/E861AIfih1−/−Adarb1−/−Gria2R/R (dKO) compared to Adar1E861A/+Ifih1−/−Adarb1+/−Gria2R/R (dHet); and d Adar1E861A/E861AIfih1−/−Adarb1−/−Gria2R/R (dKO) compared to Adar1+/+Ifih1−/−Adarb1−/−Gria2R/R (Adar2−/−); n = 3 per genotype; red indicated FDR < 0.05. e Comparison of the differential gene expression signatures of the E861A (a) and dKO (c) samples. The increased expression of the transcripts highlighted in blue is shared between murine and human ADAR1 mutants. Top panel: y-axis has the gene expression comparison of the Adar1E861A/E861A vs WT; x-axis has the gene expression comparison of the Adar1E861A/E861AAdarb1−/− (dKO) vs dHet. Lower panel: Adar1E861A/E861A compared to Adar1E861A/E861AAdar2−/− (dKO) with expanded view of the upper right quadrant. f QuSAGE pathway analysis of the consensus interferon-stimulated gene (ISG)/cytokine signature defined by Liu et al. [20] for the Adar1E861A/E861A compared to Adar1+/+Ifih1−/− (left panel), Adarb1−/− compared to dHet (center panel), and Adar1E861A/E861AAdarb1−/− compared to dHet (dKO; right panel); log2FC, P value and FDR as indicated on each panel