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Originally published as Genetics Published Articles Ahead of Print on August 24, 2007.
Genetics, Vol. 177, 1031-1041, October 2007, Copyright © 2007
doi:10.1534/genetics.107.077925
Molecular Evolution of Pathogenicity-Island Genes in Pseudomonas viridiflava
Hitoshi Araki*,
,1,
Hideki Innan
,
Martin Kreitman* and
Joy Bergelson*
* Department of Ecology and Evolution, University of Chicago, Chicago, Illinois 60637, Department of Biology, Nanjing University, Nanjing 210093, China and Graduate University of Advanced Studies, Hayama 240-0193, Japan
1 Corresponding author: Department of Zoology, Oregon State University, 3029 Cordley Hall, Corvallis, OR 97331.
E-mail: arakih{at}science.oregonstate.edu
The bacterial pathogen Pseudomonas viridiflava possesses two pathogenicity islands (PAIs) that share many gene homologs, but are structurally and phenotypically differentiated (T-PAI and S-PAI). These PAIs are paralogous, but only one is present in each isolate. While this dual presence/absence polymorphism has been shown to be maintained by balancing selection, little is known about the molecular evolution of individual genes on the PAIs. Here we investigate genetic variation of 12 PAI gene loci (7 on T-PAI and 5 on S-PAI) in 96 worldwide isolates of P. viridiflava. These genes include avirulence genes (hopPsyA and avrE), their putative chaperones (shcA and avrF), and genes encoding the type III outer proteins (hrpA, hrpZ, and hrpW). Average nucleotide diversities in these genes (
= 0.004–0.020) were close to those in the genetic background. Large numbers of recombination events were found within PAIs and a sign of positive selection was detected in avrE. These results suggest that the PAI genes are evolving relatively freely from each other on the PAIs, rather than as a single unit under balancing selection. Evolutionarily stable PAIs may be preferable in this species because preexisting genetic variation enables P. viridiflava to respond rapidly to natural selection.