Fig. 1: CHD7 curtails RNF8/RNF168-dependent recruitment of 53BP1.
From: CHD7 and 53BP1 regulate distinct pathways for the re-ligation of DNA double-strand breaks
a Schematic representation of the 53BP1 gain-of-function screen to reveal rescue phenotypes from experimentally evoked compromised recruitment of 53BP1 to sites of DNA damage. b Representative immunofluorescent images from the screen showing lack of 53BP1 nuclear body and foci formation in U2OS-shRNF168 cells upon induction of the shRNA. c Experimental design of the 53BP1 gain-of-function RNAi screen. d, e The average number of 53BP1 and γH2AX foci per nucleus upon the indicated siRNA-mediated depletions in the U2OS-shRNF168 background. f Quantification of single-cell QIBC analysis of >1000 cells per plasmid transfection. U2OS cells were treated with the indicated siRNAs and transfected with the indicated siRNA-resistant GFP–CHD7 fusions. Cells were exposed to 0.5 Gy of IR and 53BP1 foci were quantified after 15 min in control cells (GFP-negative) and CHD7-transfected (GFP-positive) cells. Mean (solid line) and standard deviation from the mean (dashed lines) are indicated. Scale bar 10 µm. Source data are provided as a Source Data file.
