We have used recombineering to mutate the chromosomal lacZ gene of E. Coli in order to generate a library of 17 tester strains which each reverts to wild type by a different mechanism. Our library improves upon previous libraries in that it is entirely chromosomal, covers all 6 base substitutions, 6 short (1 or 2nt) insertion/deletion events, as well as template switch events associated with direct repeats and with hairpins caused by imperfect inverted repeats (quasipalindromes). Quasipalindrome associated templated mutations are responsible for the hottest natural mutational hotspots in the E. Coli genome, and are responsible for about half of all carcinogenic mutations in humans and yet their mechanism is not well understood. Using our quasipalindrome reporter strains, we show that the mutations associated with quasipalindromes are affected by the direction of the replication fork and are prevented by 3' exonucleases. We investigate the anti-HIV drug azidothymidine (AZT) and find that it promotes template switching at both direct repeats and quasipalndromes.