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Pseudomonas amygdali  pv.  tabaci  (formerly  Pseudomonas syringae  pv.  tabaci ; Pta) is a gram‐negative bacterium that causes bacterial wildfire disease in  Nicotiana tabacum . The pathogen establishes infections by using a type III secretion system to inject type III effector proteins (T3Es) into cells, thereby interfering with the host__s immune system. To counteract the effectors, plants have evolved disease‐resistance genes and mechanisms to induce strong resistance on effector recognition. By screening a series of Pta T3E‐deficient mutants, we have identified HopAZ1 as the T3E that induces disease resistance in  N. tabacum  ‘N509’. Inoculation with the Pta ∆ hopAZ1  mutant did not induce resistance to Pta in N509. We also found that the Pta ∆ hopAZ1  mutant did not induce a hypersensitive response and promoted severe disease symptoms in N509. Furthermore, a C‐terminal truncated HopAZ1 abolished HopAZ1‐dependent cell death in N509. These results indicate that HopAZ1 is the avirulence factor that induces resistance to Pta by N509.

molecular plant pathology

HopAZ1, a type III effector of  Pseudomonas amygdali  pv.  tabaci , induces a hypersensitive response in tobacco wildfire‐resistant  Nicotiana tabacum  ‘N509’