The Plant Pathogen Pseudomonas syringae pv. tomato Is Genetically Monomorphic and under Strong Selection to Evade Tomato Immunity

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

Pest and disease management: why we shouldn’t go against the grain

Citation: Skelsey, P, . . . & Garrett, K. (2013). Pest and Disease Management: Why We Shouldn't Go against the Grain. PLoS One, 8(9), e75892. https://doi.org/10.1371/journal.pone.0075892Given the wide range of scales and mechanisms by which pest or disease agents disperse, it is unclear whether there might exist a general relationship between scale of host heterogeneity and spatial spread that could be exploited by available management options. In this model-based study, we investigate the interaction between host distributions and the spread of pests and diseases using an array of models that encompass the dispersal and spread of a diverse range of economically important species: a major insect pest of coniferous forests in western North America, the mountain pine beetle (Dendroctonus ponderosae); the bacterium Pseudomonas syringae, one of the most-widespread and best-studied bacterial plant pathogens; the mosquito Culex erraticus, an important vector for many human and animal pathogens, including West Nile Virus; and the oomycete Phytophthora infestans, the causal agent of potato late blight. Our model results reveal an interesting general phenomenon: a unimodal (‘humpbacked’) relationship in the magnitude of infestation (an index of dispersal or population spread) with increasing grain size (i.e., the finest scale of patchiness) in the host distribution. Pest and disease management strategies targeting different aspects of host pattern (e.g., abundance, aggregation, isolation, quality) modified the shape of this relationship, but not the general unimodal form. This is a previously unreported effect that provides insight into the spatial scale at which management interventions are most likely to be successful, which, notably, do not always match the scale corresponding to maximum infestation. Our findings could provide a new basis for explaining historical outbreak events, and have implications for biosecurity and public health preparedness