Fig. 1: FAM111A deficiency sensitizes cells to PARPis and CPT.
From: FAM111A protects replication forks from protein obstacles via its trypsin-like domain

a Knockout of FAM111A by CRISPR/Cas9 (set 1 gRNA). Parental HAP1 (WT) and FAM111A KO clones (KO #14 and #16) were analyzed for the indicated proteins by Western blotting. *, truncated FAM111A protein. b Clonogenic survival assays. Cells analyzed in a were cultured in the presence of the indicated concentration of niraparib or CPT for 6 days. For ionizing radiation (IR), cells were irradiated at the indicated doses and cultured for 6 days. Results shown are representative of three independent experiments and values are mean ± s.d. of technical replicates (n = 3). p values were calculated relative to FAM111A WT. ****p < 0.0001; n.s. not significant (two-tailed unpaired t-test). c Analyses of cell death by Annexin V/PI staining. After treatment with 1 µM niraparib or DMSO for 48 h, cells stained with Annexin V-APC and PI were analyzed by flow cytometry. Results shown are representative of three independent experiments and percentages of cells in each quadrant are indicated. d Quantification of Annexin V-positive cells. Experiments were performed as in c. Values are mean ± s.d. of independent experiments (n = 3). **p < 0.01 (two-tailed unpaired t-test). Source data are provided as a Source Data file.