Abstract
Thousands of apurinic/apyrimidinic (AP or abasic) sites form in each cell, each day. This simple DNA lesion can have profound consequences to cellular function, genome stability, and disease. As potent blocks to polymerases, they interfere with the reading and copying of the genome. Since they provide no coding information, they are potent sources of mutation. Due to their reactive chemistry, they are intermediates in the formation of lesions that are more challenging to repair including double-strand breaks, interstrand crosslinks, and DNA protein crosslinks. Given their prevalence and deleterious consequences, cells have multiple mechanisms of repairing and tolerating these lesions. While base excision repair of abasic sites in double-strand DNA has been studied for decades, new interest in abasic site processing has come from more recent insights into how they are processed in single-strand DNA. In this review, we discuss the source of abasic sites, their biological consequences, tolerance mechanisms, and how they are repaired in double and single-stranded DNA.