Apoptotic DNA fragmentation is a key feature of apoptosis. Induction of apoptosis has been recognized as a possible outcome of DNA damage by many researchers. Unicellular organisms respond to the presence of DNA lesions by activating cell cycle checkpoint and repair mechanisms, while multicellular animals have acquired the further option of eliminating damaged cells by triggering apoptosis. The intranuclear mechanisms that signal apoptosis after DNA damage overlap with those that initiate cell cycle arrest and DNA repair, and the early events in these pathways are highly conserved. In addition, multiple independent routes have recently been identified by which nuclear DNA damage can be signaled to the mitochondria, tipping the balance in favor of cell death rather than repair and survival.

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