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. 2013 Jun 10;110(26):10640–10645. doi: 10.1073/pnas.1220662110

Fig. 6.

Fig. 6.

FIGNL1 and KIAA0146 are components of the H2AX-dependent DNA damage response and HR repair pathway. (A) FIGNL1 is retained at sites of DNA damage in an H2AX-dependent manner. H2AX−/− and H2AX+/+ MEFs were infected with lentiviral plasmids encoding SFB-tagged FIGNL1. (B) BRCA2, XRCC3, or RAD51C depletion does not affect FIGNL1 foci formation after IR treatment. (C) FIGNL1 depletion does not impair RAD51 foci formation after DNA damage. The quantification of foci-positive cells was performed by counting a total of 200 cells per sample. Data are presented as mean ± SD from three different experiments. (D) The knockdown of FIGNL1 and RAD51AP1 in DR-GFP U2OS cells was confirmed with immunoblotting. (E) FIGNL1 and RAD51AP1 depletion has an additive effect on HR repair. Data are presented as mean ± SD from three different experiments. (F) FIGNL1 and RAD51AP1 depletion have an additive effect on cell sensitivity after IR treatment. Data are presented as mean ± SD from three different experiments. (G) A proposed model for FIGNL1-containing protein complex in DNA damage response and homologous recombination repair. Details in the text. Ctrl, control; IB, immunoblotting.