Fig. 7: Differing roles of BRCA2, FANCA and RAD52 in preventing DSB-induced mutations. | Nature Communications

Fig. 7: Differing roles of BRCA2, FANCA and RAD52 in preventing DSB-induced mutations.

From: iMUT-seq: high-resolution DSB-induced mutation profiling reveals prevalent homologous-recombination dependent mutagenesis

Fig. 7

A Metagene line plot of base substitution and deletion rates delta to -DSB and then delta to control siRNA. B Same as (A) but for FANCA siRNA. C Same as (A) but for BRCA2 siRNA. D Heatmap of deletion rates per DSB loci of different deletion types, delta to -DSB then delta to control siRNA. E Immunofluorescence of U2OS cells treated with 5 μM etoposide for 1 hr followed by a 3 hr recovery period, probing for RPA70 and RAD51 with either control, BRCA2 or FANCA siRNA treatment, scalebar is 5 µm. F Quantification of RAD51 foci per nucleus in immunofluorescence from (E), lines represent median and interquartile ranges, statistics done using an unpaired, two-sided Wilcoxon test, *** p < 0.001, n = 296, 307 and 228 nuclei respectively across 3 independent biological replicates. G Same as (F) but for RPA70 foci per nucleus, n = 251, 309 and 326 nuclei respectively across 3 independent biological replicates. H Heatmaps of translocation rates for RAD51, FANCA, BRCA2 and RAD52 depletions, each row and each column represent different loci that are either HR or NHEJ-prone with each cell being the translocation rate the two loci, delta to control siRNA. I Average translocation rate between different DSB loci prone to either HR or NHEJ or uncut control loci, with depletion of BRCA2, FANCA, RAD52 or RAD51, points represent each biological replicate and error bars are S.D., all statistics done relative to CTRLsi using paired, two-sided t-tests, * p < 0.05, ** p < 0.01, n = 6 independent biological replicates for CTRLsi and 3 for all other conditions. Source data and statistics are provided with this paper.

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