ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks

ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks

ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks, Published online: 08 January 2019; doi:10.1038/s41467-018-07729-2

Mutations in the ATM tumor suppressor gene confer hypersensitivity to DNA-damaging chemotherapeutic agents. Here, the authors provide evidence that these hypersensitivities reflect a crucial role for ATM at damaged replication forks being to prevent toxic DNA end-joining leading to chromosome fusions and cell death.

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