Fig. 3 | Nature Communications

Fig. 3

From: A licensing step links AID to transcription elongation for mutagenesis in B cells

Fig. 3

The RR domain is necessary for AID Igh targeting and for genome-wide DNA damage. a (Left) Mutation profiles throughout the Sμ region schematized above, from all analysed sequences. The number and frequency (mutations per base pair) of mutations scored are indicated. (Middle) Pie charts of mutation load per sequence; slices represent proportion of sequences with the indicated number of mutations, with the total number of sequences analysed shown in the centre. (Right) Bar plots of proportion of mutations (Muts) at C:G within WRC (W = A/T, R = A/G) motifs or not or at A:T pairs. b Competitive growth of AID-deficient CH12 B cells complemented with AID variants-ires-GFP or empty vector (GFP), co-cultured with untransduced cells (GFP). Cultures were treated with either DMSO or 1 nM Did B. Mean GFP+/GFP ratio ± s.d. over time from three independent experiments are shown relative to day 0. c Mutagenic activity of AID7.3 variants in E. coli, measured by the relative frequency of rifampicin resistance (Rif-R). Means (bars) of median values (dots) from 2 independent experiments (5 cultures/experiment) are shown, normalized to AID. d CSR activity of AID or AID7.3 variants-ires-GFP in AID-deficient CH12 B cells, as the proportion of IgA+ cells in GFP+ population (minus background) 72 h post-activation. Means (bars) from 2 to 4 independent experiments (dots), normalized to AID. e SHM activity, estimated from IgM-loss over time in DT40 Aicda−/− ΔΨVλ B cells complemented with AID variants-ires-GFP, 1 of the 2 independent experiments is shown. f Effect of AID or AID7.3 variants-ires-GFP on competitive growth of transduced AID-deficient CH12 B cells. Means GFP+/GFP ratio ± s.d. over time from three independent experiments, each normalized to maximal value

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