Abstract
SummaryCrop disease outbreaks are often associated with clonal expansions of single pathogenic lineages. To determine whether similar boom-and-bust scenarios hold for wild pathosystems, we carried out a multi-year, multi-site survey of Pseudomonas in its natural host Arabidopsis thaliana. The most common Pseudomonas lineage corresponded to a ubiquitous pathogenic clade. Sequencing of 1,524 genomes revealed this lineage to have diversified approximately 300,000 years ago, containing dozens of genetically identifiable pathogenic sublineages. There is differentiation at the level of both gene content and disease phenotype, although the differentiation may not provide fitness advantages to specific sublineages. The coexistence of sublineages indicates that in contrast to crop systems, no single strain has been able to overtake the studied A. thaliana populations in the recent past. Our results suggest that selective pressures acting on a plant pathogen in wild hosts are likely to be much more complex than those in agricultural systems.
Highlights
In agricultural and clinical settings, pathogenic colonizations are frequently associated with expansions of a small number of genetically identical microbial lineages (Butler et al, 2013; Cai et al, 2011; Kolmer, 2005; Park et al, 2015; Yoshida et al, 2013)
Dozens of Pseudomonas operational taxonomical units (OTUs) Persist in A. thaliana Populations To obtain a first understanding of local diversity of Pseudomonas, which is abundant in A. thaliana populations from Southwestern Germany (Agler et al, 2016), we analyzed the v3-v4 region of 16S rDNA sequences from epi- and endophytic leaf compartments, across six host populations in spring and fall of three consecutive years (Figures 1A and S1A; Table S1)
Thirteen of the 56 OTUs, including the most abundant OTU, OTU5, were classified as P. viridiflava, which belongs to the P. syringae complex
Summary
In agricultural and clinical settings, pathogenic colonizations are frequently associated with expansions of a small number of genetically identical microbial lineages (Butler et al, 2013; Cai et al, 2011; Kolmer, 2005; Park et al, 2015; Yoshida et al, 2013) While such epidemics are favored by low genetic diversity of the host (Zhu et al, 2000) and absence of competing microbes (Brown et al, 2013), many, if not most, pathogens can colonize host populations that are both genetically diverse and can accommodate a diversity of other microbes (Falkinham et al, 2015; Woolhouse et al, 2001). What has become clear is that non-epidemic pathogens are phenotypically polymorphic, but the underlying scale and pattern of genetic and genomic differentiation remain unknown (Kniskern et al, 2011; Thrall et al, 2001)
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