Neisseria gonorrhoeae is an etiological agent of gonorrhea, which remains a global health problem. This bacterium possesses MutL and MutS DNA repair proteins encoded by
mutL and
mutS genes, whose inactivation causes a mutator phenotype. We have demonstrated the differential gene expression in
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Neisseria gonorrhoeae is an etiological agent of gonorrhea, which remains a global health problem. This bacterium possesses MutL and MutS DNA repair proteins encoded by
mutL and
mutS genes, whose inactivation causes a mutator phenotype. We have demonstrated the differential gene expression in
N. gonorrhoeae mutL and
mutS mutants using DNA microarrays. A subset of differentially expressed genes encodes proteins that can influence adhesion and biofilm formation. Compared to the wild-type strain,
N. gonorrhoeae mutL and
mutS mutants formed denser biofilms with increased biofilm-associated biomass on the abiotic surface. The
N. gonorrhoeae mutS::km, but not the
mutL mutant, was also more adherent and invasive to human epithelial cells. Further, during infection of epithelial cells with
N. gonorrhoeae mutS::km, the expression of some bacterial genes encoding proteins that can influence gonococcal adhesion was changed compared with their expression in cells infected with the wild-type gonococcus, as well as of human genes’ encoding receptors utilized by
N. gonorrhoeae (CD46, CEACAM 1, HSPG 2). Thus, deficiency in the
mutS gene resulting in increased mutation frequency in singular organisms can be beneficial in populations because these mutants can be a source of features linked to microbial fitness.
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