Abstract
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.
Highlights
Neisseria gonorrhoeae is a human-specific, gram-negative diplococcus that causes the sexually transmitted disease gonorrhea
N. gonorrhoeae interacts with host epithelial cells using multistep adhesion as the key stage of infection, allowing biofilm formation, which is an important virulence factor [6,7]
Our results indicated that N. gonorrhoeae with a disrupted mutS gene formed denser biofilms and was more adherent and invasive to human epithelial cells compared to the wild-type strain
Summary
Neisseria gonorrhoeae (gonococcus) is a human-specific, gram-negative diplococcus that causes the sexually transmitted disease gonorrhea. Gonococcal infections remain a global health issue, as highlighted by the World Health Organization, which has recently classified N. gonorrhoeae as a “priority pathogen” due to spreading multidrug resistance and increasing infection incidence [1,2]. Gonococcal infection may increase the risk of human immunodeficiency virus transmission [3,4,5]. DNA repair systems are crucial in all living organisms. MutL and MutS proteins are conserved DNA repair molecules present at all domains of life. MutL is a “molecular matchmaker”, which mediates the protein–protein interactions during mismatch recognition and strand removal, and MutS recognizes unpaired and mispaired bases and small insertion/deletion loops in duplex DNA [8]. In N. gonorrhoeae, inactivation of mutL and mutS genes leads to an overall increase in mutability
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