The Genetics of Neisseria Species

Abstract

Neisseria gonorrhoeae and Neisseria meningitidis are closely related organisms that cause the sexually transmitted infection gonorrhea and serious bacterial meningitis and septicemia, respectively. Both species possess multiple mechanisms to alter the expression of surface-exposed proteins through the processes of phase and antigenic variation. This potential for wide variability in surface-exposed structures allows the organisms to always have subpopulations of divergent antigenic types to avoid immune surveillance and to contribute to functional variation. Additionally, the Neisseria are naturally competent for DNA transformation, which is their main means of genetic exchange. Although bacteriophages and plasmids are present in this genus, they are not as effective as DNA transformation for horizontal genetic exchange. There are barriers to genetic transfer, such as restriction-modification systems and CRISPR loci, that limit particular types of exchange. These host-restricted pathogens illustrate the rich complexity of genetics that can help define the similarities and differences of closely related organisms.

Kinetics of DNA uptake during transformation provide evidence for a translocation ratchet mechanism

“…1B). In all of our strains (Table S1) recA expression is repressed to inhibit gene conversion in the pilin locus (35). Using uncoated beads that were treated like DNA-coated beads but without adding DNA, only 7% of the attempts resulted in binding, indicating that binding was mostly specific to DNA.…”

DprA is required for natural transformation and affects pilin variation in Neisseria gonorrhoeae

“…However, we found that dprA mutants exhibited increased RecA-dependent pilin variation compared to isogenic parental strains (Figs 3 and 4) suggesting a possible role of DprA in modulating this process. RecA-dependent pilin variation at the pilE locus in Neisseria has been the focus of intense research for decades [reviewed in Cahoon & Seifert (2011) and Rotman & Seifert (2014)] and current models invoke numerous recombination proteins (RecA, RecX, RecO, RecR, RecJ, RecQ, RecG, RuvABC) and the formation of quadraduplex DNA to initiate the non-reciprocal recombination process. Several components of the mismatch correction system have been shown to modulate pilin antigenic variation although the precise mechanism remains unknown (Criss et al, 2010).…”

“…Models of pilin variation invoke a double-strand break at the pilE locus resulting in a single strand invading the pilS locus (Rotman & Seifert, 2014). Therefore, it is possible that DprA binds this small singlestrand fragment during strand invasion and inhibits the formation of heteroduplex thereby reducing gene conversion and pilin variation.…”

“…The role of DprA in transformation [reviewed in Johnston et al (2014) and Rotman & Seifert (2014)] has been studied in several species of naturally transforming bacteria including B. subtilis (Tadesse & Graumann, 2007;Yadav et al, 2014), S. pneumoniae (Mirouze et al, 2013;MortierBarriere et al, 2007;Quevillon-Cheruel et al, 2012), Heli. pylori (Smeets et al, 2000;Zhang & Blaser, 2012) and C. jejuni (Takata et al, 2005).…”

“…Twitching motility is mediated by the depolymerization of pilus oligomers to promote pilus retraction and DNA transport (Wolfgang et al, 1998). In N. gonorrhoeae and Neisseria meningitidis, TFP undergo pilus phase variation and pilin antigenic variation, which function in immune evasion [reviewed in Rotman & Seifert (2014)]. …”