Open AccessHopAZ1, a type III effector of Pseudomonas amygdali pv. tabaci , induces a hypersensitive response in tobacco wildfire‐resistant Nicotiana tabacum ‘N509’
Author(s) -
Kashihara Sachi,
Nishimura Takafumi,
Noutoshi Yoshiteru,
Yamamoto Mikihiro,
Toyoda Kazuhiro,
Ichinose Yuki,
Matsui Hidenori
Publication year - 2022
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/mpp.13198
Subject(s) - pseudomonas syringae , nicotiana tabacum , biology , effector , hypersensitive response , mutant , microbiology and biotechnology , pathogen , nicotiana , type three secretion system , plant disease resistance , gene , genetics , solanaceae
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.