ArticleMolecular plant pathology2022
HopAZ1, a type III effector of Pseudomonas amygdali pv. tabaci, induces a hypersensitive response in tobacco wildfire-resistant Nicotiana tabacum 'N509'.
Article in Molecular plant pathology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Pseudomonas syringae pv. tabaci 8018 is Virulent Against Tobacco Cultivars N509 and Burley21 Due to Spontaneous Mutation in hopAZ1.Molecular plant pathology · 2026Article
- Comparative Genomic Analysis Identifies FleQ and GcbB as Virulence-Associated Factors in Pseudomonas syringae pv. tabaci Strains.Molecular plant pathology · 2025Article
- Pseudomonas syringae pv. tabaci 6605 Requires Seven Type III Effectors to Infect Nicotiana benthamiana.Molecular plant pathology · 2025Article
- Genomic Islands of Pseudomonas syringae pv. tabaci 6605: Identification of PtaGI-1 as a Pathogenicity Island With Effector Genes and a Tabtoxin Cluster.Molecular plant pathology · 2025Article
- Membrane vesicle engineering with "à la carte" bacterial-immunogenic molecules for organism-free plant vaccination.Microbial biotechnology · 2023Review
- The RING-Finger Protein NbRFP1 Contributes to Regulating the Host Hypersensitive Response Induced by Oat Dwarf Virus RepA.International journal of molecular sciences · 2023Article
- HopAZ1, a type III effector of Pseudomonas amygdali pv. tabaci, induces a hypersensitive response in tobacco wildfire-resistant Nicotiana tabacum 'N509'.Molecular plant pathology · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
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Abstract
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.
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