ArticleMolecular plant pathology2020
AvrE1 and HopR1 from Pseudomonas syringae pv. actinidiae are additively required for full virulence on kiwifruit.
Article in Molecular plant pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- The AcWRKY40-AcICS1 Module Regulates Kiwifruit Resistance to Pseudomonas syringae pv. actinidiae via Salicylic Acid Synthesis.Plant, cell & environment · 2026Article
- Article
- Multiple effectors trigger non-host resistance in Solanum americanum against Pseudomonas syringae.The Plant journal : for cell and molecular biology · 2025Article
- Pseudomonas syringae pv. tabaci 6605 Requires Seven Type III Effectors to Infect Nicotiana benthamiana.Molecular plant pathology · 2025Article
- AmBio · 2025Article
- Genomic Biosurveillance of the Kiwifruit Pathogen Pseudomonas syringae pv. actinidiae Biovar 3 Reveals Adaptation to Selective Pressures in New Zealand Orchards.Molecular plant pathology · 2025Article
- Identification and Characterization of Innate Immunity in Actinidia melanandra in Response to Pseudomonas syringae pv. actinidiae.Plant, cell & environment · 2025Article
- The flavonoid metabolic pathway genes Ac4CL1, Ac4CL3 and AcHCT1 positively regulate the kiwifruit immune response to Pseudomonas syringae pv. actinidiae.Plant molecular biology · 2025Article
- Individually redundant effectors are collectively required for bacterial pathogen virulence.The ISME journal · 2025Article
- Comparative genomic analyses provide insight into the pathogenicity of three Pseudomonas syringae pv. actinidiae strains from Anhui Province, China.BMC genomics · 2024Article
- Genetic dissection of the tissue-specific roles of type III effectors and phytotoxins in the pathogenicity of Pseudomonas syringae pv. syringae to cherry.Molecular plant pathology · 2024Article
- The role of the type VI secretion system in the stress resistance of plant-associated bacteria.Stress biology · 2024Review
- EnhancingFrontiers in plant science · 2024Article
- Article
- Bacterial pathogens deliver water/solute-permeable channels as a virulence strategy.bioRxiv : the preprint server for biology · 2023Article
- Article
- Large-Scale Transposon Mutagenesis Reveals Type III Secretion Effector HopR1 Is a Major Virulence Factor inPlants (Basel, Switzerland) · 2022Article
- Effector loss drives adaptation of Pseudomonas syringae pv. actinidiae biovar 3 to Actinidia arguta.PLoS pathogens · 2022Article
- Metaeffector interactions modulate the type III effector-triggered immunity load of Pseudomonas syringae.PLoS pathogens · 2022Article
- Complete genome sequence of the kiwifruit bacterial canker pathogen Pseudomonas savastanoi strain MHT1.BMC microbiology · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pseudomonas syringae pv. actinidiae ICMP 18884 biovar 3 (Psa3) produces necrotic lesions during infection of its kiwifruit host. Bacterial growth in planta and lesion formation are dependent upon a functional type III secretion system (T3S), which translocates multiple effector proteins into host cells. Associated with the T3S locus is the conserved effector locus (CEL), which has been characterized and shown to be essential for the full virulence in other P. syringae pathovars. Two effectors at the CEL, hopM1 and avrE1, as well as an avrE1-related non-CEL effector, hopR1, have been shown to be redundant in the model pathogen P. syringae pv. tomato DC3000 (Pto), a close relative of Psa. However, it is not known whether CEL-related effectors are required for Psa pathogenicity. The Psa3 allele of hopM1, and its associated chaperone, shcM, have diverged significantly from their orthologs in Pto. Furthermore, the CEL effector hopAA1-1, as well as a related non-CEL effector, hopAA1-2, have both been pseudogenized. We have shown that HopM1 does not contribute to Psa3 virulence due to a truncation in shcM, a truncation conserved in the Psa lineage, probably due to the need to evade HopM1-triggered immunity in kiwifruit. We characterized the virulence contribution of CEL and related effectors in Psa3 and found that only avrE1 and hopR1, additively, are required for in planta growth and lesion production. This is unlike the redundancy described for these effectors in Pto and indicates that these two Psa3 genes are key determinants essential for kiwifruit bacterial canker disease.
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