Many pathogenic bacteria express pili (fimbriae) on their cell surfaces. These structures mediate binding of bacteria to host tissues, and may also be involved in other aspects of pathogenesis. Neisseria gonorrhoeae pili are mainly composed of a single protein, pilin, whose expression is controlled at chromosomal expression loci (pilE)1 An intact pilin gene and promoter sequences2-5 are only found at pilE. Strain MS 11 contains two expression sites (pilEl and pilE2)1,2, whereas several of its derivatives5 and other clinical isolates4 contain only one. Silent pilin loci (pilS1-pilS7) contain truncated variant pilin genes lacking the promoter and conserved pilin gene sequences3,6. Pilin antigenic variation in N. gonorrhoeae occurs by DNA recombination between one of the silent partial variant gene segments in pilS and an expressed pilin gene in pilE7,8. The recombination reactions are nonreciprocal, and therefore the mechanism has been classified as gene conversion. We report that much of the recombination between pilin loci actually occurs after transformation of living piliated cells by DNA liberated from lysed cells within a population. This constitutes a new molecular mechanism for an antigenic variation system, as well as the first specific function for a DNA transformation system.
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