Fig. 3

DSB repair improvement by acceptor–donor cell interaction depends on ATM kinase activity. a Residual, 24–h 53BP1 foci in ATMwt fibroblasts (acceptor) pretreated with DNA–PK or ATM inhibitors, irradiated with 6–Gy x–rays and subsequently cultured alone or in co–culture with untreated MiaPaCa–2 cells (donor). DMSO used as control. b Residual, 24–h 53BP1 foci numbers in 6–Gy irradiated ATMwt or ATM^−/− fibroblasts (acceptor) grown in mono– or co–culture with untreated MiaPaCa–2 cells (donor). c Normalized residual 53BP1 foci numbers in 6–Gy irradiated MiaPaCa–2 cells (acceptor) in mono– or co–culture with either ATMwt or ATM^−/− fibroblasts (donor) or ATMwt fibroblasts pretreated with ATM inhibitor (DMSO used as control). d Comparison of 53BP1 foci numbers in 6–Gy irradiated MiaPaCa–2 cells (acceptor) cultured either alone or in co–culture with untreated MiaPaCa–2 cells, Capan1 cells, ATMwt or ATM^−/− fibroblasts (donors). Number of analysed irradiated acceptor cells is n = 30, unless otherwise indicated. Data represent mean ± SD (two–sided t–test; ns, not significant, **P < 0.01, ***P < 0.005)