title: The plant pathogen Pseudomonas syringae pv. tomato is genetically monomorphic and under strong selection to evade tomato immunity.
abstract: Recently, genome sequencing of many isolates of genetically monomorphic bacterial human pathogens has given new insights into pathogen microevolution and phylogeography. Here, we report a genome-based micro-evolutionary study of a bacterial plant pathogen, Pseudomonas syringae pv. tomato. Only 267 mutations were identified between five sequenced isolates in 3,543,009 nt of analyzed genome sequence, which suggests a recent evolutionary origin of this pathogen. Further analysis with genome-derived markers of 89 world-wide isolates showed that several genotypes exist in North America and in Europe indicating frequent pathogen movement between these world regions. Genome-derived markers and molecular analyses of key pathogen loci important for virulence and motility both suggest ongoing adaptation to the tomato host. A mutational hotspot was found in the type III-secreted effector gene hopM1. These mutations abolish the cell death triggering activity of the full-length protein indicating strong selection for loss of function of this effector, which was previously considered a virulence factor. Two non-synonymous mutations in the flagellin-encoding gene fliC allowed identifying a new microbe associated molecular pattern (MAMP) in a region distinct from the known MAMP flg22. Interestingly, the ancestral allele of this MAMP induces a stronger tomato immune response than the derived alleles. The ancestral allele has largely disappeared from today's Pto populations suggesting that flagellin-triggered immunity limits pathogen fitness even in highly virulent pathogens. An additional non-synonymous mutation was identified in flg22 in South American isolates. Therefore, MAMPs are more variable than expected differing even between otherwise almost identical isolates of the same pathogen strain.
authors: Department of Plant Pathology, Physiology, and Weed Science, Virginia Tech, Blacksburg, Virginia, United States of America.
authors: Rongman
authors: R
authors: Cai
authors: James
authors: J
authors: Lewis
authors: Shuangchun
authors: S
authors: Yan
authors: Haijie
authors: H
authors: Liu
authors: Christopher R
authors: CR
authors: Clarke
authors: Francesco
authors: F
authors: Campanile
authors: Nalvo F
authors: NF
authors: Almeida
authors: David J
authors: DJ
authors: Studholme
authors: Magdalen
authors: M
authors: Lindeberg
authors: David
authors: D
authors: Schneider
authors: Massimo
authors: M
authors: Zaccardelli
authors: Joao C
authors: JC
authors: Setubal
authors: Nadia P
authors: NP
authors: Morales-Lizcano
authors: Adriana
authors: A
authors: Bernal
authors: Gitta
authors: G
authors: Coaker
authors: Christy
authors: C
authors: Baker
authors: Carol L
authors: CL
authors: Bender
authors: Scotland
authors: S
authors: Leman
authors: Boris A
authors: BA
authors: Vinatzer
mesh_terms: D000483:Alleles; D017931:DNA Primers; D005060:Europe; D005408:Flagellin / Q000235:genetics / Q000378:metabolism; D018506:Gene Expression Regulation, Plant; D056426:Genetic Loci; D005819:Genetic Markers; D054884:Host-Pathogen Interactions; D018551:Solanum lycopersicum / Q000382:microbiology*; D009154:Mutation; D009656:North America; D058974:Phylogeography; D010935:Plant Diseases / Q000382:microbiology*; D057865:Plant Immunity; D018515:Plant Leaves; D020641:Polymorphism, Single Nucleotide; D044224:Pseudomonas syringae / Q000235:genetics* / Q000472:pathogenicity*; D017422:Sequence Analysis, DNA; D037521:Virulence Factors / Q000235:genetics*
chemical_list: D017931:DNA Primers; D005819:Genetic Markers; D037521:Virulence Factors; D005408:Flagellin