DNA repair::Mycobacterium tuberculosis


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DNA repair As an intracellular pathogen M. tuberculosis is exposed to a variety of DNA damaging assaults, primarily from host-generated antimicrobial toxic radicals. Exposure to reactive oxygen species and/or reactive nitrogen species causes different types of DNA damage including oxidation, depurination, methylation and deamination that can give rise to single- and double-strand breaks (DSBs).

DnaE2 polymerase is upregulated in M. tuberculosis by several DNA damaging agents as well as during infection of mice.<ref name=Boshoff>{{#invoke:Citation/CS1|citation |CitationClass=journal }}</ref> Loss of this DNA polymerase reduces the virulence of M. tuberculosis in mice.<ref name=Boshoff /> DnaE2 is an error-prone repair DNA repair polymerase that appears to contribute to M. tuberculosis survival during infection.

The two major pathways employed in repair of DSBs are homologous recombinational repair (HR) and non-homologous end joining (NHEJ). Macrophage-internalized M. tuberculosis is able to persist if either of these pathways is defective, but is attenuated when both pathways are defective.<ref name=Brzostek>{{#invoke:Citation/CS1|citation |CitationClass=journal }}</ref> This indicates that intracellular exposure of M. tuberculosis to reactive oxygen and/or reactive nitrogen species results in the formation of DSBs that are repaired by HR or NHEJ.<ref name=Brzostek /> However deficiency of DSB repair does not appear to impair M. tuberculosis virulence in animal models.<ref name="pmid24842925">{{#invoke:Citation/CS1|citation |CitationClass=journal }}</ref>

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DNA repair
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