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. 2021 Apr 20;118(17):e2024258118. doi: 10.1073/pnas.2024258118

Fig. 3.

Fig. 3.

DDX11 helicase activity averts DNA damage accumulation and damage sensitivity. (A) Western blot analysis of U2OS Ctrl and DDX11 KO cells complemented with EV, WT DDX11, DDX11 helicase dead (K50R), mutation in Iron–Sulfur cluster domain (R263Q), and DDX11-Timeless interaction defective motif (KAE). (Right) Schematic representation of DDX11 and its associated mutations. (B) Cell viability of U2OS Ctrl and DDX11 KO cells complemented with EV and DDX11 variants upon mitomycin C and olaparib drug treatment. Cell viability was measured using crystal violet after 5 d of incubation in the presence of the drugs at the indicated concentrations (n = 3). Error bar shows average ± SEM. (C) Quantification and representative micrographs of 53BP1 and γ-H2AX foci in U2OS Ctrl and DDX11 KO cells complemented with different DDX11 variants after 24 h of recovering from 1 h treatment with cisplatin (2 μM). (Scale bar, 10 μm.) n = 2. Statistical analysis was performed using Student’s t test. Error bar shows average ± SD.