Modelling the impacts of pests and diseases on agricultural systems

The current status on the taxonomy of Pseudomonas revisited: An update.

Pseudomonas syringae is a phytopathogenic bacterium that causes diseases of monocots, herbaceous dicots, and woody dicots, worldwide On woody plants, reports of disease due to P syringae have markedly increased in the last years and the diseases have been recognized as a major threat to the primary products of agroforestry practices Detection in Italy of a new highly aggressive population of P syringae in 2008 on kiwifruit, which caused severe epidemics in the following years throughout the kiwifruit-growing areas of Asia, Europe, Oceania, and South America, rendered the entire kiwifruit industry vulnerable to the disease Similarly, occurrence of an aggressive population of P syringae on horse chestnut in 2002 in the Netherlands has rapidly established itself as a major threat to horse chestnut throughout Northwest Europe To better understand the origin of such disease epidemics, a thorough knowledge of the pathogen is needed in sensu lato  Here, we report the most important features of the pathogen and its hosts in an attempt to clarify some key aspects In particular, the diseases and the economic losses they cause, disease epidemiology, pathogen diversity, and the possible means of disease control have been discussed throughout the manuscript In addition to the ability to cause the disease, the damage caused to woody plants through the ice nucleation activity of this bacterium is discussed

/pdf/disease-and-frost-damage-of-woody-plants-caused-by-wmpa89l0c2.pdf

Disease and Frost Damage of Woody Plants Caused by Pseudomonas syringae: Seeing the Forest for the Trees

Phytopathogenic bacteria possess an arsenal of effector proteins that enable them to subvert host recognition and manipulate the host to promote pathogen fitness. The type III secretion system (T3SS) delivers type III-secreted effector proteins (T3SEs) from bacterial pathogens such as Pseudomonas syringae, Ralstonia solanacearum, and various Xanthomonas species. These T3SEs interact with and modify a range of intracellular host targets to alter their activity and thereby attenuate host immune signaling. Pathogens have evolved T3SEs with diverse biochemical activities, which can be difficult to predict in the absence of structural data. Interestingly, several T3SEs are activated following injection into the host cell. Here, we review T3SEs with documented enzymatic activities, as well as T3SEs that facilitate virulence-promoting processes either indirectly or through non-enzymatic mechanisms. We discuss the mechanisms by which T3SEs are activated in the cell, as well as how T3SEs modify host targets to promote virulence or trigger immunity. These mechanisms may suggest common enzymatic activities and convergent targets that could be manipulated to protect crop plants from infection.

What the Wild Things Do: Mechanisms of Plant Host Manipulation by Bacterial Type III-Secreted Effector Proteins.

Comparative genomic analysis of Erwinia amylovora reveals novel insights in phylogenetic arrangement, plasmid diversity, and streptomycin resistance

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. Copyright: ß 2013 McCann et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. " PBR and MDT are joint senior authors on this work.

Correction: Genomic Analysis of the Kiwifruit Pathogen pv. Provides Insight into the Origins of an Emergent Plant Disease.

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Correction: Genomic Analysis of the Kiwifruit Pathogen pv. Provides Insight into the Origins of an Emergent Plant Disease.