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BIOLOGICAL SCIENCES / POPULATION BIOLOGY
Just one cross appears capable of dramatically altering the population biology of a eukaryotic pathogen like Toxoplasma gondii





*Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305;
Department of Pathology, Cambridge University, Cambridge CB2 1QP, United Kingdom;
Wellcome Trust Sanger Institute, Hinxton CB10 1SA, United Kingdom;
Institute for Genomic Research, Rockville, MD 20850; ¶Department of Biology and Penn Genomics Institute, University of Pennsylvania, Philadelphia, PA 19104; ||Department of Molecular Microbiology, Center for Infectious Diseases, Washington University School of Medicine, St. Louis, MO 63110; and **Department of Veterinary Molecular Biology, Montana State University, Bozeman, MT 59717
Edited by Louis H. Miller, National Institutes of Health, Rockville, MD, and approved May 24, 2006 (received for review November 29, 2005)
Toxoplasma gondii, an obligate intracellular protozoan of the phylum Apicomplexa, is estimated to infect over a billion people worldwide as well as a great many other mammalian and avian hosts. Despite this ubiquity, the vast majority of human infections in Europe and North America are thought to be due to only three genotypes. Using a genome-wide analysis of single-nucleotide polymorphisms, we have constructed a genealogy for these three lines. The data indicate that types I and III are second- and first-generation offspring, respectively, of a cross between a type II strain and one of two ancestral strains. An extant T. gondii strain (P89) appears to be the modern descendant of the non-type II parent of type III, making the full genealogy of the type III clonotype known. The simplicity of this family tree demonstrates that even a single cross can lead to the emergence and dominance of a new clonal genotype that completely alters the population biology of a sexual pathogen.
clonal population structure | genetic recombination | virulence
Conflict of interest statement: No conflicts declared.
This paper was submitted directly (Track II) to the PNAS office.
Data deposition: The sequences reported in this paper have been deposited in the GenBank database (accession nos. DQ676958DQ676977 and DQ768301DQ768304).

To whom correspondence should be addressed. E-mail: john.boothroyd{at}stanford.edu
© 2006 by The National Academy of Sciences of the USA
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