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Antigenic variation through targeted DNA rearrangements provides a powerful diversity generating mechanism that allows a variety of pathogens to stay one step ahead of acquired immunity in their hosts. The Lyme disease spirochete encodes such a system that is required for persistent infection. The  vls  locus, carried on a 29 kb linear plasmid (lp28-1) in the type strain B31, carries 15 silent cassettes from which information is unidirectionally transferred into the expression locus,  vlsE.  Recent studies have surprisingly shown that, with the exception of the RuvAB branch migrase, no other known recombination/repair proteins appear to play a role in the recombinational switching process. In the work presented here we show that G4 DNA can be formed by sequences within the B31  vlsE  locus, prompting us to investigate the presence of potential G4-forming DNA throughout the  vls  locus of several Lyme spirochete strains and species. We found that runs of G, three nucleotides and longer occur at a very high density, with a greater than 100-fold strand-specific distribution in the  vls  locus of three  B. burgdorferi  strains as well as in  B. afzelii and B. garinii,  in spite of the bias for the use of A-T rich codons in  Borrelia  species. Our findings suggest the possibility that G4 DNA may be a mediator of recombinational switching at the  vlsE  locus in the Lyme spirochetes.

Suggested Role for G4 DNA in Recombinational Switching at the Antigenic Variation Locus of the Lyme Disease Spirochete