An Alternative DNA Structure Is Necessary for Pilin Antigenic Variation in Neisseria gonorrhoeae

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Science  07 Aug 2009:
Vol. 325, Issue 5941, pp. 764-767
DOI: 10.1126/science.1175653

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Taking Shape

DNA recombination mechanisms enable certain pathogens to modify the proteins on their outer surfaces by rearranging their genes and so avoid repeated detection by the immune system. Cahoon and Seifert (p. 764) have found that antigenic variation of a single genetic locus in the human pathogen Neisseria gonorrhoeae is triggered by a specific cis-acting DNA element. This 16–base pair DNA sequence formed an unusual DNA structure in vitro; a guanine quartet (G4), which has been implicated in only a few other biological processes. The G4 forming sequence is required for processing the gene conversion reaction leading to antigenic variation. These findings have implications both for understanding mechanisms of DNA recombination and its role in microbial pathogenesis.


Pathogens can use DNA recombination to promote antigenic variation (Av) of surface structures to avoid immune detection. We identified a cis-acting DNA sequence near the antigenically variable pilin locus of the human pathogen, Neisseria gonorrhoeae. This 16–base pair guanine (G)–rich sequence was required for pilin Av and formed a guanine quartet (G4) structure in vitro. Individual mutations that disrupted the structure also blocked pilin Av and prevented nicks required for recombination from occurring within the G4 region. A compound that binds and stabilizes G4 structures also inhibited pilin Av and prevented nicks from occurring on the G-rich strand. This site constitutes a recombination initiation sequence/structure that directs gene conversion to a specific chromosomal locus.

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