Abstract
It is well known that the high fidelity of DNA replication in eucaryotes results in part from the accuracy by which DNA polymerases copy the base sequences in DNA. It is also well known that the reactions of many mutagens and carcinogens with DNA result in the formation of bulky adducts. Experimental evidence indicates that these bulky adducts block DNA synthesis in vitro and in vivo.1 A paradox in mutagenesis is how DNA polymerases, with their stringent requirement for correct base pairing, can accommodate bulky adducts to yield mutations in nascent DNA. One possibility is that the adducts responsible for mutagenesis are labile and form non-bulky intermediary products that are mutagenic. We have proposed that apurinic sites are mutagenic intermediates2 and we have subsequently analyzed their mutagenic potential in vivo and in vitro.
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