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J. Bacteriol. doi:10.1128/JB.01301-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Population Genetics and Linkage Analysis of Loci Within the FCT Region of Streptococcus pyogenes

Department of Microbiology and Immunology, New York Medical College, Valhalla, NY, USA 10595

^* To whom correspondence should be addressed. Email: debra_bessen{at}nymc.edu.

	Abstract

The FCT-regions of Streptococcus pyogenes strains encode a variety of cell wall-anchored surface proteins that bind the extracellular matrix of the human host and/or give rise to pilus-like appendages. Strong linkage is evident between transcription regulatory loci positioned within the FCT- and emm-regions, and the emm pattern genotype marker for preferred infection at the throat or skin. These findings provide a basis for the hypothesis that FCT-region gene products contribute to tissue-specific infection. In an initial series of steps to address this possibility, FCT-regions of 13 strains underwent comparative sequence analysis, the gene content of the FCT-region was characterized for 113 strains via PCR, and genetic linkage was assessed. A history of extensive recombination within FCT-regions was evident. The emm pattern D-defined skin specialist strains were highly homogenous in their FCT-region gene content, whereas the emm pattern A-C-defined throat specialist strains displayed a greater variety of forms. Most pattern A-C strains harbored prtF1 (75%) but lacked cpa (75%). In contrast, the majority of emm pattern D strains had cpa (92%) but lacked prtF1 (79%). Models based on FCT- and emm-region genotypes revealed the most parsimonious pathways of evolution. Using niche-determining candidate genes to infer phylogeny, emm pattern E strains - the so-called generalists which lack a strong tissue site preference - occupied a transition zone separating most throat specialists from skin specialists. Overall, population genetic analysis supports the possibility that the FCT-region gives rise to surface proteins that are largely necessary, but not always sufficient, for conferring tissue site preference for infection.

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