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

McCann, H. C., Rikkerink, E. H. A., Bertels, F., Fiers, M., Lu, A., George, J.-R.-., et al. (2013). Genomic analysis of the kiwifruit pathogen Pseudomonas syringae pv. actnidiae provides insight into the origins of an emergent plant disease. PLoS Pathogens, 9(7): e1003503. doi:10.1371/journal.ppat.1003503.

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 Creators:
McCann, Honour C., Author
Rikkerink, Erik H. A., Author
Bertels, Frederic1, Author                 
Fiers, Mark, Author
Lu, Ashley, Author
George, Jonathan Rees-, Author
Andersen, Mark T., Author
Gleave, Andrew P., Author
Haubold, Bernhard2, Author           
Wohlers, Mark W., Author
Guttman, David S., Author
Wang, Pauline W., Author
Straub, Christina, Author
Vanneste, Joel L., Author
Rainey, Paul B.3, Author                 
Templeton, Matthew D., Author
Affiliations:
1External Organizations, ou_persistent22              
2Research Group Bioinformatics, Department Evolutionary Genetics, Max Planck Institute for Evolutionary Biology, Max Planck Society, ou_1445644              
3External Scientific Member Group Experimental and Evolutionary Genetics, Max Planck Institute for Evolutionary Biology, Max Planck Society, ou_1445637              

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 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.

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Language(s): eng - English
 Dates: 2013-01-202013-05-282013-07-252013
 Publication Status: Issued
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: DOI: 10.1371/journal.ppat.1003503
 Degree: -

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Title: PLoS Pathogens
  Other : PLoS Pathog.
Source Genre: Journal
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Publ. Info: San Francisco, CA : Public Library of Science
Pages: - Volume / Issue: 9 (7) Sequence Number: e1003503 Start / End Page: - Identifier: ISSN: 1553-7366 (print)
ISSN: 1553-7374 (online)
CoNE: https://pure.mpg.de/cone/journals/resource/1000000000018830