The way cells respond to radiation or chemical exposure that damages deoxyribonucleic acid (DNA) is important because induced lesions left unrepaired, or those that are misrepaired, can lead to mutation, cancer, or lethality. Prokaryotic and eukaryotic cells have evolved mechanisms that repair damaged DNA directly, such as nucleotide excision repair, base excision repair, homology-based recombinational repair, or nonhomologous end joining, which promote survival and reduce potential deleterious effects (1 ). However, at least eukaryotic cells also have cell cycle checkpoints capable of sensing DNA damage or blocks in DNA replication, signaling the cell cycle machinery, and causing transient delays in progression at specific phases of the cell cycle (2 ;seeref.3 for a review). A related but more primitive system may exist in prokaryotes (4 –7 ). These delays are thought to provide cells with extra time for mending DNA lesions before entry into critical phases of the cell cycle, such as S or M, events that could be lethal with damaged DNA.
