Abstract
Vascular plant pathogens travel long distances through host veins, leading to life-threatening, systemic infections. In contrast, nonvascular pathogens remain restricted to infection sites, triggering localized symptom development. The contrasting features of vascular and nonvascular diseases suggest distinct etiologies, but the basis for each remains unclear. Here, we show that the hydrolase CbsA acts as a phenotypic switch between vascular and nonvascular plant pathogenesis. cbsA was enriched in genomes of vascular phytopathogenic bacteria in the family Xanthomonadaceae and absent in most nonvascular species. CbsA expression allowed nonvascular Xanthomonas to cause vascular blight, while cbsA mutagenesis resulted in reduction of vascular or enhanced nonvascular symptom development. Phylogenetic hypothesis testing further revealed that cbsA was lost in multiple nonvascular lineages and more recently gained by some vascular subgroups, suggesting that vascular pathogenesis is ancestral. Our results overall demonstrate how the gain and loss of single loci can facilitate the evolution of complex ecological traits.
Highlights
Pathogenic microorganisms cause diseases of animals and plants
We identified two ortholog groups (OGs) whose presence was strongly associated with the distribution of tissue-specific lifestyles
To experimentally test the alternate models, we examined the effects of manipulating cbsA on the contrasting tissue-specific behavior of two closely related barley pathogens from the same species: vascular Xanthomonas translucens pvs. translucens (Xtt) and nonvascular undulosa (Xtu)
Summary
Pathogenic microorganisms cause diseases of animals and plants. Some pathogenic species colonize the host vasculature, which leads to systemic infection, while others remain localized to nonvascular tissues. Transitions between plant pathogenic and commensal Pseudomonas [5], transitions between mutualist and parasitic phenotypes in nitrogen-fixing bacteria [6, 7], and transitions between mutualistic and plant pathogenic Rhodococcus [8] have all been shown to reproducibly occur through the gain and loss of genomic islands containing multiple genes all contributing to the same phenotype. These rapid evolutionary dynamics have profound implications for our understanding of disease ecology and disease management strategies
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