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. 2022 Aug 15;119(34):e2207408119. doi: 10.1073/pnas.2207408119

Fig. 3.

Fig. 3.

Mutations in the RPA32 interacting domain of XPA lead to a cellular defect in the repair of UV lesions. (A) Expression level of WT and RPA32-interaction mutant XPA in XP2OS cells transduced with HA-tagged XPA. Proteins were detected anti-XPA and anti-HA antibodies, using Ku80 as a loading control. (B) Clonogenic survival assays. Cells were treated with the indicated UV dose, grown for 10 d, and stained with methylene blue. Survival rates were normalized to nontreated cells. (C) Quantification of C: 100 cells were counted for each sample and the data represent at least two independent experiments. The P value was compared to XPA WT. (D) Determination of CPD repair kinetics using slot-blot assays. Cells were irradiated with 5 J/m2 genomic DNA isolated, and adduct levels determined with an anti-CPD antibody. Data were normalized to WT at 0 h. The P value was measured compared to XPA WT. **P < 0.01, ***P < 0.001.