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.

维管植物病原体通过宿主静脉长距离传播，导致危及生命的全身感染。相反，非血管病原体仍然局限于感染部位，引发局部症状发展。血管和非血管疾病的对比特征表明不同的病因，但每种疾病的基础仍不清楚。在这里，我们表明水解酶 CbsA 作为维管植物和非维管植物发病机制之间的表型转换。cbsA在黄单胞菌科的维管植物病原菌基因组中富集，而在大多数非维管物种中不存在。CbsA 表达允许非血管黄单胞菌引起血管枯萎病，而cbsA诱变导致血管或非血管症状发展的减少。系统发育假设检验进一步表明，cbsA在多个非血管谱系中丢失，最近在一些血管亚群中获得，表明血管发病机制是祖先的。我们的结果总体上证明了单个基因座的获得和损失如何促进复杂生态特征的进化。