19 research outputs found

    Field studies evaluate methods to prevent sudden oak death in oaks and tanoak

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    We conducted field studies to evaluate management methods for the prevention of sudden oak death (SOD), caused by Phytophthora ramorum. Phosphite was applied as a trunk spray at the product label rate (22.36% a.i. aqueous solution + Pentra-Bark® surfactant at 2.3% v/v) to a 1.35 ha block of 233 large-diameter (mean 46 cm) tanoaks. Annual phosphite applications began in 2008; symptoms of P. ramorum were not seen in the stand until 2011. In 2013, SOD incidence in treated trees was 32% compared to 18% in adjacent untreated trees. Subsequent discontinuation of phosphite treatment did not affect disease progress; SOD continued to increase at similar rates in phosphite-treated and control trees, reaching 47% among phosphite-treated trunks compared to 32% in untreated trunks. Preventative phosphite application did not delay SOD onset, or reduce SOD incidence or SOD-related mortality. In contrast, in other studies we found that removal of California bay (Umbellularia californica) around coast live oaks (Quercus agrifolia), California black oaks (Q. kelloggii), and Shreve oaks (Q. parvula var. shrevei) strongly decreased or prevented new disease development over study periods ranging from 5 to 7 years. In these studies, SOD incidence in oaks treated by removal of nearby California bay was 20 to 25% lower than in untreated controls

    Host-induced aneuploidy and phenotypic diversification in the Sudden Oak Death pathogen Phytophthora ramorum

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    BackgroundAneuploidy can result in significant phenotypic changes, which can sometimes be selectively advantageous. For example, aneuploidy confers resistance to antifungal drugs in human pathogenic fungi. Aneuploidy has also been observed in invasive fungal and oomycete plant pathogens in the field. Environments conducive to the generation of aneuploids, the underlying genetic mechanisms, and the contribution of aneuploidy to invasiveness are underexplored. We studied phenotypic diversification and associated genome changes in Phytophthora ramorum, a highly destructive oomycete pathogen with a wide host-range that causes Sudden Oak Death in western North America and Sudden Larch Death in the UK. Introduced populations of the pathogen are exclusively clonal. In California, oak (Quercus spp.) isolates obtained from trunk cankers frequently exhibit host-dependent, atypical phenotypes called non-wild type (nwt), apparently without any host-associated population differentiation. Based on a large survey of genotypes from different hosts, we previously hypothesized that the environment in oak cankers may be responsible for the observed phenotypic diversification in P. ramorum.ResultsWe show that both normal wild type (wt) and nwt phenotypes were obtained when wt P. ramorum isolates from the foliar host California bay (Umbellularia californica) were re-isolated from cankers of artificially-inoculated canyon live oak (Q. chrysolepis). We also found comparable nwt phenotypes in P. ramorum isolates from a bark canker of Lawson cypress (Chamaecyparis lawsoniana) in the UK; previously nwt was not known to occur in this pathogen population. High-throughput sequencing-based analyses identified major genomic alterations including partial aneuploidy and copy-neutral loss of heterozygosity predominantly in nwt isolates. Chromosomal breakpoints were located at or near transposons.ConclusionThis work demonstrates that major genome alterations of a pathogen can be induced by its host species. This is an undocumented type of plant-microbe interaction, and its contribution to pathogen evolution is yet to be investigated, but one of the potential collateral effects of nwt phenotypes may be host survival
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