Genomic Analysis of the Kiwifruit Pathogen Pseudomonas syringae pv. actinidiae Provides Insight into the Origins of an Emergent Plant Disease

PLoS Pathogens

Ashley Lu¹  Joel Vanneste²  Christina Straub²  Erik H. A. Rikkerink²  David S. Guttman³  Paul B. Rainey⁴  Honour C. McCann⁴  Mark Fiers⁴  Bernhard Haubold⁵  Mark W. Wohlers⁵  Andrew P. Gleave⁵  Frederic Bertels⁵  Pauline W. Wang⁵  Jonathan Rees-George⁶  Mark T. Andersen⁶  Matthew D. Templeton⁷ 

[1] Biozentrum, University of Basel and Swiss Institute of Bioinformatics, Basel, Switzerland;Centre for the Analysis of Genome Evolution and Function, University of Toronto, Toronto, Canada;Max Planck Institute for Evolutionary Biology, Plön, Germany;New Zealand Institute for Advanced Study and Allan Wilson Centre, Massey University, Auckland, New Zealand;The New Zealand Institute for Plant and Food Research Limited, Auckland, New Zealand;The New Zealand Institute for Plant and Food Research Limited, Lincoln, New Zealand;The New Zealand Institute for Plant and Food Research Limited, Ruakura, Hamilton, New Zealand

关键词: Pseudomonas syringae;    Leaves;    Gene conversion;    Phylogenetics;    Evolutionary genetics;    Comparative genomics;    Population genetics;    Plant pathology;   

DOI  :  10.1371/journal.ppat.1003503

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

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.

【 授权许可】

CC BY