Abstract
One reason for the rise of bacterial antibiotic resistance is acquisition of new mutations through DNA damage. Lesions on the DNA obstruct regular DNA replication polymerases. Upon DNA damage, cells induce the DNA damage response; one effect is an increase in DNA damage tolerance because they recruit Y family DNA polymerases with active sites large enough to bypass lesions. However, Y family DNA polymerases have low fidelity and may lead to errors in replication and thus mutations, some of which may result in antibiotic resistance. In Escherichia coli, there are two such polymerases, Pol IV and Pol V, the latter being the most error prone. In Acinetobacter baumannii there are multiple genes encoding DNA Pol V, and these are organized as operons (as well as unlinked genes). The multiple copies may be active in A. baumannii, and the activities of the products they encode may be comparable to their counterparts in E. coli. The operons and unlinked genes coding for Pol V in A. baumannii will be characterized to determine if their activities differ to the single operon in E. coli.
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