Genomic analysis of the Kiwifruit pathogen Pseudomonas syringae pv. actinidiae provides insight into the origins of an emergent plant disease

PLoS Pathog. 2013;9(7):e1003503. doi: 10.1371/journal.ppat.1003503. Epub 2013 Jul 25.

Abstract

The origins of crop diseases are linked to domestication of plants. Most crops were domesticated centuries--even millennia--ago, thus limiting opportunity to understand the concomitant emergence of disease. Kiwifruit (Actinidia spp.) is an exception: domestication began in the 1930s with outbreaks of canker disease caused by P. syringae pv. actinidiae (Psa) first recorded in the 1980s. Based on SNP analyses of two circularized and 34 draft genomes, we show that Psa is comprised of distinct clades exhibiting negligible within-clade diversity, consistent with disease arising by independent samplings from a source population. Three clades correspond to their geographical source of isolation; a fourth, encompassing the Psa-V lineage responsible for the 2008 outbreak, is now globally distributed. Psa has an overall clonal population structure, however, genomes carry a marked signature of within-pathovar recombination. SNP analysis of Psa-V reveals hundreds of polymorphisms; however, most reside within PPHGI-1-like conjugative elements whose evolution is unlinked to the core genome. Removal of SNPs due to recombination yields an uninformative (star-like) phylogeny consistent with diversification of Psa-V from a single clone within the last ten years. Growth assays provide evidence of cultivar specificity, with rapid systemic movement of Psa-V in Actinidia chinensis. Genomic comparisons show a dynamic genome with evidence of positive selection on type III effectors and other candidate virulence genes. Each clade has highly varied complements of accessory genes encoding effectors and toxins with evidence of gain and loss via multiple genetic routes. Genes with orthologs in vascular pathogens were found exclusively within Psa-V. Our analyses capture a pathogen in the early stages of emergence from a predicted source population associated with wild Actinidia species. In addition to candidate genes as targets for resistance breeding programs, our findings highlight the importance of the source population as a reservoir of new disease.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actinidia / growth & development
  • Actinidia / microbiology*
  • Bacterial Proteins / chemistry
  • Bacterial Proteins / genetics*
  • Bacterial Proteins / metabolism
  • Crops, Agricultural / growth & development
  • Crops, Agricultural / microbiology
  • Fruit / growth & development
  • Fruit / microbiology
  • Genome, Bacterial*
  • Genomic Islands
  • Italy
  • Japan
  • New Zealand
  • Phylogeny
  • Plant Diseases / etiology
  • Plant Diseases / microbiology*
  • Plant Shoots / growth & development
  • Plant Shoots / microbiology
  • Polymorphism, Single Nucleotide
  • Pseudomonas syringae / genetics*
  • Pseudomonas syringae / growth & development
  • Pseudomonas syringae / isolation & purification
  • Pseudomonas syringae / pathogenicity
  • Recombination, Genetic
  • Republic of Korea
  • Species Specificity
  • Virulence

Substances

  • Bacterial Proteins

Grants and funding

This work was funded in part by the New Zealand Ministry for Business, Innovation and Employment (www.mbie.govt.nz) contract C06X0812 (to MDT and EHAR), and Allan Wilson Centre for Molecular Ecology and Evolution (http://www.allanwilsoncentre.ac.nz/) (to PBR). PBR is grateful for support from Zespri International, Mt Maunganui, New Zealand (http://www.Zespri.com). The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.