The complete genome sequence of a relatively weak virulent tobacco pathogen, Pseudomonas syringae pv. tabaci 8018 ( Pta 8018) was determined to elucidate key genetic elements that cause disease. Genome comparison of Pta 8018 to the previously available P. syringae pv. tabaci strains revealed that Pta 8018 and Pta 11528 had high genome synteny, with an approximately 5 Mb chromosome inversion in Pta 6605. Furthermore, Pta 8018 had lost the pathogenicity island GI‐1 including a tabtoxin biosynthesis gene cluster and showed weak virulence on Nicotiana tabacum ‘Xanthi NC’ (Xanthi). When inoculated into several tobacco cultivars, Pta 8018 caused leaf angular spot not only in Xanthi but also in N. tabacum cultivars Burley21 and N509, while Pta 6605 did not cause disease in Burley21 and N509 due to the presence of avirulence factor HopAZ1. We found that a mutation in hopAZ1 allows Pta 8018 to avoid recognition in these cultivars. Introduction of intact hopAZ1 of Pta 6605 into Pta 8018 rendered it avirulent to N509 and Burley21, revealing that effector HopAZ1 is a key virulence determinant of P. syringae pv. tabaci . Our data show that although Pta 8018 has reduced virulence strength by the loss of GI‐1 in Xanthi, it expanded its host range to two other cultivars through mutation of hopAZ1 .
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HIRAKI et al. (2026) studied this question.
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