DNA transformation leads to pilin antigenic variation in Neisseria gonorrhoeae

Abstract

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). An intact pilin gene and promoter sequences are only found at pilE. Strain MS11 contains two expression sites (pilE1 and pilE2), whereas several of its derivatives and other clinical isolates contain only one. Silent pilin loci (pilS1-pilS7) contain truncated variant pilin genes lacking the promoter and conserved pilin gene sequences. Pilin antigenic variation in N. gonorrhoeae occurs by DNA recombination between one of he silent partial variant gene segments in pilS and an expressed pilin gene in pilE. 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.

Structure of the Bundle-forming Pilus from Enteropathogenic Escherichia coli

“…1A). In contrast, the second loop (68 -80) connecting ␣2 to the ␤-sheet possesses a short 3 10 (25, 39 -41). Instead they are arranged in a complex mixed ␤-sheet topology, with the following strand order ␤2/␤3/␤1 (Fig.…”

Identification of Epitopes Recognized by Monoclonal Antibodies SM1 and SM2 Which React with All Pili of Neisseria gonorrhoeae but Which Differentiate between Two Structural Classes of Pili Expressed by Neisseria meningitidis and the Distribution of Their Encoding Sequences in the Genomes of Neisseria spp.

“…Experience with non-reverting P-derivatives of gonococci in which pilin and N-terminal coding sequences are deleted Segal et al, 1985) suggests that class I1 meningococcal strains with either type of residual class I pi1 sequences are unlikely to be able to regain the ability to produce class I pili. However, it is conceivable, by analogy with gonococci (Seifert et al, 1988), that defects in class I pilin production might be repaired following the acquisition of a complete complement of pilE sequences by transformation. Nevertheless, these strains have probably elaborated class I pili at some stage in their evolutionary history.…”

The organisation of the multigene family which encodes the major cell surface protein, pMGA, of Mycoplasma gallisepticum

“…Perhaps most notable of all in respect of pMGA coding sequences 1. l-l .6 is the absence of internal stop codons which might have been expected had the pMGA system been functionally analogous to the pilin system of N. gonorrhoeae, the genome of which encodes multiple pilin gene variants, many of which contain one or more premature stop codons [6]. Clearly M. gallisepticum pMGA genes are under considerable selective pressure to maintain their ability to encode viable polypeptides rather than to simply act as an inert reservoir of sequence variability as is the case of N. gonorrhoeae pilin variants.…”