Abstract
Mutagenesis by AID: Being in the Right Place at the Right Time
Highlights
Abundant during S phase, the main role of uracil-DNA glycosylase (UNG) is to remove uracil misincorporated during DNA replication, but it can act at other times, both on double and single stranded DNA
The new study by Le and Maizels fully explains these results by demonstrating that the enforced presence of activationinduced cytidine deaminase (AID) in the nucleus is toxic in S phase
Mutagenesis induced by AID results from a plethora of misfortunes, from simple miscoding by uracil/abasic sites to mismatch-induced error-prone repair or the generation of double strand breaks (DSBs) resolved with loss of genetic information by the non-homologous end joining (NHEJ) pathway
Summary
Abundant during S phase, the main role of UNG is to remove uracil misincorporated during DNA replication, but it can act at other times, both on double and single stranded DNA (dsDNA and ssDNA, respectively). Cells have a back up glycosylase, SMUG1 [1], that removes uracil from double stranded DNA, a pathway ideally suited to faithfully repair deaminated cytosines outside replication.
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