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Letter

Evolution of Chlamydia trachomatis diversity occurs by widespread interstrain recombination involving hotspots

¹ Center for Immunobiology and Vaccine Development, Children’s Hospital Oakland Research Institute, Oakland California 94609, USA; ² Centro de Bacteriologia, Instituto Nacional de Saúde, Lisboa 1649-016, Portugal; ³ T-10 Theoretical Biology and Biophysics, MS-K710 Los Alamos National Laboratory, Los Alamos, New Mexico 87545, USA; ⁴ Department of Medicine and Biomedical Sciences, University of California at San Francisco School of Medicine, San Francisco, California 94143, USA

Chlamydia trachomatis is an obligate intracellular bacterium of major public health significance, infecting over one-tenth of the world’s population and causing blindness and infertility in millions. Mounting evidence supports recombination as a key source of genetic diversity among free-living bacteria. Previous research shows that intracellular bacteria such as Chlamydiaceae may also undergo recombination but whether this plays a significant evolutionary role has not been determined. Here, we examine multiple loci dispersed throughout the chromosome to determine the extent and significance of recombination among 19 laboratory reference strains and 10 present-day ocular and urogenital clinical isolates using phylogenetic reconstructions, compatibility matrices, and statistically based recombination programs. Recombination is widespread; all clinical isolates are recombinant at multiple loci with no two belonging to the same clonal lineage. Several reference strains show nonconcordant phylogenies across loci; one strain is unambiguously identified as recombinantly derived from other reference strain lineages. Frequent recombination contrasts with a low level of point substitution; novel substitutions relative to reference strains occur less than one per kilobase. Hotspots for recombination are identified downstream from ompA, which encodes the major outer membrane protein. This widespread recombination, unexpected for an intracellular bacterium, explains why strain-typing using one or two genes, such as ompA, does not correlate with clinical phenotypes. Our results do not point to specific events that are responsible for different pathogenicities but, instead, suggest a new approach to dissect the genetic basis for clinical strain pathology with implications for evolution, host cell adaptation, and emergence of new chlamydial diseases.

E-mail ddean{at}chori.org; fax: (510) 450-7910.

[Supplemental material is available online at www.genome.org. The sequence data from this study have been submitted to GenBank under accession numbers: AY884090–AY884108 (for pmpA), AY884109–AY884127 (for pmpB), AY299408–AY299426 (for pmpD), AY967735–AY967738 (for pmpE), AY887644–AY887662 and DQ065739– DQ065748 (for pmpF), AY967739–AY967757 (for pmpG), AY967759–AY967761 (for pmpH), AY299427–AY299445 (for pmpI), DQ065736–DQ065738, DQ062749–DQ062755, and DQ076723–DQ076741 (for ORF CT049), DQ113596–DQ113614 and DQ076742–DQ076751 (for IGR rs2/ompA), DQ116393–DQ116402 (for ompA), DQ113625– DQ113643 and DQ113615–DQ113624 (for IGR [ompA/pbpB]), DQ151840 (for ORF CT166), DQ151841–DQ151847 and DQ239937–DQ239957 (for rs2), DQ151848–DQ151854 (for yfh0_1 and IGR [yfh0_1/parB]). Clinical isolates have the following designation in GenBank: C/CL-1 (CS-362-07), Da/CL-2 (CS-431/04), E/CL-3 (I-174), G/CL-4 (CS-490/95), G/CL-5 (I-149), H/CL-6 (CS-121/96), H/CL-7 (I-139), I/CL-8 (I-24), Ia/CL-9 (CS-190/96), and Ja/CL-10 (S-91).]

Article published online before print. Article and publication data are at http://www.genome.org/cgi/doi/10.1101/gr.5674706

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