Fig. 3: Loss of KLF5 induces DNA damage and genomic instability upon ATRi.
From: KLF5 loss sensitizes cells to ATR inhibition and is synthetic lethal with ARID1A deficiency
a Bar graphs showing percentages of cells in each cell cycle phase based on EdU and DAPI staining of WT and KLF5 KO U2-OS cells treated with DMSO or ATRi (biological n = 3). b Bar graphs showing percentages of EdU positive WT and KLF5 KO U2-OS cells following ATRi treatment. Cells were labelled with 10 μM EdU for 30 min prior to fixation. Data are shown as means ± SEM; biological n = 3. c FACS plots showing the percentages of γH2AX positive cells in WT and KLF5 KO U2-OS cells untreated or following ATRi treatment at indicated timepoints. d As in (c), except cells were treated with CHK1i. Percentages of γH2AX positive cells are shown in red. e Percentages of γH2AX positive S phase cells following ATRi (1 μM or 2 μM for 24 h) treatment (biological n = 3). f Percentages of γH2AX positive S phase cells following CHK1i (100 nM or 200 nM for 2 h) treatment (biological n = 3). g Left, mean numbers of micronuclei per cell following 24 h treatment with DMSO or 1 μM ATRi in WT and KLF5 KO U2-OS cells (biological n = 6). Right, representative images showing micronuclei indicated with white arrows, scale bars = 10 μm. All data are represented as means ± SEM. Statistical analyses were performed using two-way ANOVA test (a), unpaired two-sided Student’s t-test (b, g) and one-way ANOVA test with multiple comparisons (e, f). Source data are provided as a Source Data file.
