The zinc uptake regulator (Zur) has highly conserved sequences in the plant pathogen , while its functions are diverse in different strains or races. To elucidate the functions of Zur in pv. (), we constructed a -deleted mutant (Δ) by homologous recombination. Compared with the wild type, Δ demonstrated reduced pathogenicity in the host soybean and reduced ability to trigger hypersensitive responses (HR) in nonhosts such as tobacco, tomato, chili pepper, and eggplant. Additionally, the deletion of significantly enhanced 's sensitivity to Zn, Fe, and Cu, induced an imbalance in intracellular zinc homeostasis, decreased extracellular polysaccharide (EPS) production, and down-regulated the expression of extracellular hydrolases (cellulase, endo-glucanase, amylase, and protease). Functional complementation restored the defective properties of Δ to the wild-type levels. The qRT-PCR results showed that expression was remarkably induced by Zn. Moreover, the deletion of evidently reduced the expression levels of representative genes (, , , , and ), extracellular hydrolase encoding genes (, , , , , , and ), and EPS synthesis genes (, , , , , and ) relative to the wild type. In summary, the results suggested that Zur may be involved in pathogenicity in the host soybean and in triggering HR in nonhosts of by regulating the synthesis of virulence factors and the expression of genes. This laid a foundation for further analysis of the mechanism of Zur in -plant interaction.
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