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. Author manuscript; available in PMC: 2012 Mar 7.
Published in final edited form as: DNA Repair (Amst). 2010 Dec 10;10(3):260–270. doi: 10.1016/j.dnarep.2010.11.007

Figure 8. Possible repair pathways for AZT-induced lesions in E. coli.

Figure 8

Incorporation of AZT by DNA polymerases leads to replication gaps. ExoIII can remove the 3′ AZT monophosphate moiety, leaving a clean ssDNA gap. The gap may be filled by DNA polymerase or may engage in recombinational reaction. The RecFOR proteins load RecA onto gaps, leading to induction of the SOS transcriptional response and gap-filling recombination with a sister chromosome. Alternatively, RecAFOR recombination may occur before the 3′ AZT-MP is removed; in such a case, ExoIII is required to remove AZT in the recombination intermediates or products. In the absence of RecFOR, gaps are converted to double-strand breaks by converging replication forks or by endonucleases. RecBCD nuclease processes the break, removing AZT in the process and generating recombinogenic 3′ strands onto which RecA is loaded. This RecA filament may also signal the SOS reponse. Recombination with the sister chromosome restores an intact replication fork.