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Background  DNA double strand breaks induced by DNA damaging agents, such ionizing radiation, are repaired by multiple DNA repair pathways including non-homologous end-joining (NHEJ) repair and homologous recombination (HR) repair. ATM-dependent DNA damage checkpoint regulates a part of DNA repair pathways, however, the exact role of ATM activity remains to be elucidated. In order to define the molecular structure of DNA double strand breaks requiring ATM activity we examined repair of DNA double strand breaks induced by different restriction endonucleases in normal human diploid cells treated with or without ATM-specific inhibitor.    Results  Synchronized G1 cells were treated with various restriction endonucleases. DNA double strand breaks were detected by the foci of phosphorylated ATM at serine 1981 and 53BP1. DNA damage was detectable 2 hours after the treatment, and the number of foci decreased thereafter. Repair of the 3'-protruding ends created by  Pst  I and  Sph  I was efficient irrespective of ATM function, whereas the repair of a part of the blunt ends caused by  Pvu  II and  Rsa  I, and 5'-protruding ends created by  Eco  RI and  Bam  HI, respectively, were compromised by ATM inhibition.    Conclusions  Our results indicate that ATM-dependent pathway plays a pivotal role in the repair of a subset of DNA double strand breaks with specific end structures.

Requirement of ATM-dependent pathway for the repair of a subset of DNA double strand breaks created by restriction endonucleases