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. 2019 Sep 10;47(20):10678–10692. doi: 10.1093/nar/gkz784

Figure 1.

Figure 1.

Loss of CSB impairs recruitment of BRCA1, MRE11/RAD50/NBS1 and CtIP but not RAP80 to DSBs. (A) Representative images of U2OS-265 WT cells with induction of FokI expression. Fixed cells were stained with an anti-γH2AX antibody in conjunction with an antibody against various endogenous proteins as indicated. Nuclei were stained with DAPI in blue in this and following figures. Scale bars in this and subsequent figures: 5 μm. (B) Quantification of the intensity of BRCA1 signal at the site of FokI-induced DSBs. The respective numbers of cells analyzed for U2OS-265 WT and CSB-KO were 277 and 309. Data are represented as scatter plot graphs from single experiments with the mean indicated in this and subsequent panels. The P value was determined using non-parametric Mann-Whitney rank-sum t-test in this and subsequent panels. (C) Quantification of the intensity of RAD50 signal at the site of FokI-induced DSBs. The respective numbers of cells analyzed for U2OS-265 WT and CSB-KO were 265 and 235. (D) Quantification of the intensity of MRE11 signal at the site of FokI-induced DSBs. The respective numbers of cells analyzed for U2OS-265 WT and CSB-KO were 267 and 254. (E) Quantification of the intensity of NBS1 signal at the site of FokI-induced DSBs. The respective numbers of cells analyzed for U2OS-265 WT and CSB-KO were 248 and 267. (F) Quantification of the intensity of CtIP signal at the site of FokI-induced DSBs. The respective numbers of cells analyzed for U2OS-265 WT and CSB-KO were 249 and 249. (G) Quantification of the intensity of RAP80 signal at the site of FokI-induced DSBs. The respective numbers of cells analyzed for U2OS-265 WT and CSB-KO were 309 and 356.