Résumé
Microbes cause disease in plants through two distinct processes. Vascular pathogens move through host veins leading to widespread infection, while non-vascular pathogens remain restricted to the site of infection. The systemic nature of vascular pathogenicity poses a much greater risk to host health; yet the mechanisms underpinning this lifestyle are unknown. Here, we examine the molecular and evolutionary basis for vascular athogenicity in Xanthomonas, a diverse genus of plant-associated bacteria that cause vascular and non-vascular diseases. As opposed to equally complex traits controlled by multiple loci, we identified a single gene, celA (encoding a cellobiosidase), that acts as a switch for vascular pathogenesis. Heterologous expression of celA in non-vascular Xanthomonas species resulted in pathotype conversion allowing for xylem colonization, while its deletion in vascular species resulted in the loss of xylem colonization, demonstrating that celA is both sufficient and necessary for vascular pathogenesis. We inferred several gains and losses of celA in Xanthomonas, where celA was acquired through horizontal transfer in what are now vascular lineages, and alternatively lost through transposon-mediated insertion in non-vascular lineages. The dynamic evolution of celA suggests that rather than representing evolutionary endpoints, vascular and non-vascular modes of infection exist on a continuum, and populations can easily flow from one end to another.