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. 2015 Dec 1;1:15034. doi: 10.1038/celldisc.2015.34

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Copyright © 2015 SIBS, CAS

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The role of CDC73 in HRR is independent of its transcriptional function. (a) Illustration of the siRNA-resistant CDC73, the core mutant (ΔC) and the 227X mutant. (b) Immunofluorescence of the eGFP-tagged constructs in U2OS cells in combination with DAPI (blue) and Phalloidin (red). (c) The defect in HRR as measured by the DR–GFP assay can be rescued by re-expression of a WT (*P=0.029) and the ΔC mutant. (d) PAF1 silencing does reduce HRR (*P=0.009). (e) DRB treatment (50 μm, 2 h) has the same effect on H2B mobility as CDC73 silencing (*P=0.033). (f) The CDC73-227X mutant does not rescue HRR in the DR–GFP assay (**P=8×10^-4). (g) CDC73 knockdown does not affect the expression of a number of essential genes for DNA repair and has no effect on the recruitment of BRCA1 (h). For all experiments (n⩾2). Average and s.d. are plotted. P-values are calculated with Student’s t-test and scale bars represent 50 and 10 μm.