FIGURE 1.

Schematic of the DDR to DSBs. Following DSB induction, they are recognized by sensor proteins such as the Mre11 complex. This leads to the activation of ATM and related kinases that promote rapid post-translational modifications (PTMs) on many proteins and remodeling of chromatin structure around the break sites. Effector proteins such as the Chk1 and Chk2 kinases amplify the signal and cells can activate cell cycle checkpoints, regulate transcription, translation, and metabolism, and activate the appropriate DNA repair processes. In some cellular contexts, or in the face of irreparable lesions, cells can activate apoptosis and senescence. The collective result is the prevention of genomic instability and the accompanying pathological outcomes.