Cell cycle arrest after DNA damage describes the interconnection between two complex signaling processes – DNA damage sensing and the cell cycle – by
a variety of biochemical interactions. Damage may arise from various sources, including radiation, chemical agents, or errors during DNA synthesis or cell division. The resulting damage is sensed by a signaling network that halts the cell cycle by modulating cyclin/Cdk activity. Cell cycle arrest can be transient to allow repair of DNA damage, or can persist indefinitely as a senescence-like state. This essay describes mechanisms of DNA damage-induced cell cycle arrest, their dynamics, and their effect on eventual cell fate. It also discusses mathematical modeling approaches used to gain insight into these processes.