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. 2013 Feb 28;9(2):e1003277. doi: 10.1371/journal.pgen.1003277

Figure 7. The interactions of Nbs1 FHA/BRCT domains with CtIP or with MDC1 involve different mechanisms to regulate DSB repair.

Figure 7

A. U2OS cells stably expressing control MKO or indicated shRNAs were treated with or without IR (10 Gy, recovered for 1 h), lysed, and immunoblotting was performed. B. EGFP-HR and EGFP-MMEJ assays were performed with U2OS cells stably expressing MKO or sh-MDC1. Western blotting was performed to show silencing of MDC1, with Ku70 as a loading control. C. EGFP-MMEJ assay was performed in U2OS cells expressing indicated CtIP variants, with endogenous CtIP silenced. Western blotting shows expression of HA-CtIP variants with Ku70 as a loading control. D. EGFP-MMEJ and EGFP-HR assays were performed in U2OS cells expressing Nbs1-WT-Myc or Nbs1-RRHK-Myc mutant with endogenous Nbs1 silenced. Western blotting shows expression of Nbs1-Myc variants with Ku70 as a loading control. E. A model to describe a role for CDK- and ATM-mediated phosphorylation of CtIP in the regulation of end resection and DSB repair (see Discussion).