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Abstract Potato virus Y(PVY,Potyviridae) is among the most important viral pathogens of potato. The potato resistance geneNy_tbrconfers hypersensitive resistance to the ordinary strain of PVY (PVY^O), but not the necrotic strain (PVY^N). Here, we unveil that residue 247 of PVY helper component proteinase (HCPro) acts as a central player controllingNy_tbrstrain‐specific activation. We found that substituting the serine at 247 in the HCPro of PVY^O(HCPro^O) with an alanine as in PVY^NHCPro (HCPro^N) disruptsNy_tbrrecognition. Conversely, an HCPro^Nmutant carrying a serine at position 247 triggers defence. Moreover, we demonstrate that plant defences are induced against HCPro^Omutants with a phosphomimetic or another phosphorylatable residue at 247, but not with a phosphoablative residue, suggesting that phosphorylation could modulateNy_tbrresistance. Extending beyond PVY, we establish that the same response elicited by the PVY^OHCPro is also induced by HCPro proteins from other members of thePotyviridaefamily that have a serine at position 247, but not by those with an alanine. Together, our results provide further insights in the strain‐specific PVY resistance in potato and infer a broad‐spectrum detection mechanism of plant potyvirus effectors contingent on a single amino acid residue. 

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.