Fig. 1

KDM4B accumulation at DSBs is crucial for DSB repair. (A) The indicated cells were treated with BrdU, laser microirradiated, and immunostained for KDM4B and γH2AX 30 min after microirradiation. Nuclei are counter-stained with DAPI. (B) CRISPR/Cas9-mediated knockout of KDM4B in T-47D cells. Sequencing chromatogram of cDNA shows the region with a deletion (CGCAGGG) that causes a premature stop codon at Ser37 in KDM4B-KO cells. (C) WT or KDM4B-KO MCF-7 and T-47D cells were subjected to immunoblotting with the indicated antibodies. (D) WT or KDM4B-KO T-47D cells were laser microirradiated and immunostained as in (A). (E and F) WT or KDM4B-KO T-47D (E) and MCF-7 cells (F) were irradiated and subjected to immunofluorescence analyses with the anti-γH2AX antibody at the indicated time after the IR. The number of nuclear γH2AX foci per cell is shown with means and SDs. ***P < 0.0001. Representative data 24 h after IR were shown at the bottom.