AvrE1 and HopR1 from <i>Pseudomonas syringae</i> pv. <i>actinidiae</i> are additively required for full virulence on kiwifruit

Jayaraman, Jay; Yoon, Minsoo; Applegate, Emma R.; Stroud, Erin A.; Templeton, Matthew D.

doi:10.1111/mpp.12989

Cited by 32 publications

(34 citation statements)

References 49 publications

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“…This may be attributed to the possible role of HopAU1 as a no virulence protein in the M228 T3SE repertoire. More evidences showed that three T3SEs, HopR1, AvrE1 and HopZ5, contributed almost 80% to Psa3 virulence [ 28 , 41 ], further supporting the no-virulence protein role of in Psa .…”

Section: Discussionmentioning

confidence: 91%

“…Studies on Psa T3SEs have performed subcellular localization and transient expression to select several T3SEs triggered HR in N. benthamiana [ 27 ]. In addition, AvrE1 Psa and HopR1 Psa have been shown to be essential for full virulence, while HopM1 (belonging to the AvrE/HopM family) exhibits functional redundancy [ 28 , 29 ]. Additional research has focused on the recognition mechanism of Psa T3SEs in model plants.…”

Section: Introductionmentioning

confidence: 99%

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Pseudomonas syringae pv. actinidiae Effector HopAU1 Interacts with Calcium-Sensing Receptor to Activate Plant Immunity

Zhang

Zhou

Liu

et al. 2022

IJMS

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Kiwifruit canker, caused by Pseudomonas syringae pv. actinidiae (Psa), is a destructive pathogen that globally threatens the kiwifruit industry. Understanding the molecular mechanism of plant-pathogen interaction can accelerate applying resistance breeding and controlling plant diseases. All known effectors secreted by pathogens play an important role in plant-pathogen interaction. However, the effectors in Psa and their function mechanism remain largely unclear. Here, we successfully identified a T3SS effector HopAU1 which had no virulence contribution to Psa, but could, however, induce cell death and activate a series of immune responses by agroinfiltration in Nicotiana benthamiana, including elevated transcripts of immune-related genes, accumulation of reactive oxygen species (ROS), and callose deposition. We found that HopAU1 interacted with a calcium sensing receptor in N. benthamiana (NbCaS) as well as its close homologue in kiwifruit (AcCaS). More importantly, silencing CaS by RNAi in N. benthamiana greatly attenuated HopAU1-triggered cell death, suggesting CaS is a crucial component for HopAU1 detection. Further researches showed that overexpression of NbCaS in N. benthamiana significantly enhanced plant resistance against Sclerotinia sclerotiorum and Phytophthora capsici, indicating that CaS serves as a promising resistance-related gene for disease resistance breeding. We concluded that HopAU1 is an immune elicitor that targets CaS to trigger plant immunity.

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Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Pseudomonas syringae pv. actinidiae Effector HopAU1 Interacts with Calcium-Sensing Receptor to Activate Plant Immunity

Zhang

Zhou

Liu

et al. 2022

IJMS

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“… AvrE1 KP808_06005 Pseudomonas syringae pv. Lachrymans (MAFF301315) 1571 98.6 Cytoplasm two-component system sensor histidine Required for in planta growth and lesion production [ 23 ]. HopA1 KP808_06050 Pseudomonas syringae pv.…”

Section: Resultsmentioning

confidence: 99%

Complete genome sequence of the kiwifruit bacterial canker pathogen Pseudomonas savastanoi strain MHT1

et al. 2022

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Background Pseudomonas savastanoi is an important plant pathogen that infects and causes symptoms in a variety of economically important crops, causing considerable loss of yield and quality. Because there has been no research reported to date on bacterial canker of kiwifruit (Actinidia chinensis) plants caused by P. savastanoi and, in particular, no in-depth studies of the complete genome sequence or pathogenic mechanism, long-lasting and environmentally friendly control measures against this pathogen in kiwifruit are lacking. This study therefore has both theoretical value and practical significance. Results We report the complete genome sequence of P. savastanoi strain MHT1, which was first reported as the pathogen causing bacterial canker in kiwifruit plants. The genome consists of a 6.00-Mb chromosome with 58.5% GC content and 5008 predicted genes. Comparative genome analysis of four sequenced genomes of representative P. savastanoi strains revealed that 230 genes are unique to the MHT1 strain and that these genes are enriched in antibiotic metabolic processes and metabolic pathways, which may be associated with the drug resistance and host range observed in this strain. MHT1 showed high syntenic relationships with different P. savastanoi strains. Furthermore, MHT1 has eight conserved effectors that are highly homologous to effectors from P. syringae, Pseudomonas amygdali, and Ralstonia solanacearum strains. The MHT1 genome contains six genomic islands and two prophage sequences. In addition, 380 genes were annotated as antibiotic resistance genes and another 734 as encoding carbohydrate-active enzymes. Conclusion The whole-genome sequence of this kiwifruit bacterial canker pathogen extends our knowledge of the P. savastanoi genome, sets the stage for further studies of the interaction between kiwifruit and P. savastanoi, and provides an important theoretical foundation for the prevention and control of bacterial canker.

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“…Moreover, a recent comparative transcriptional profiling exercise revealed that T3SS genes were strongly activated in Psa3 responding to apoplast-like conditions, compared with those in Psa1 and Psa2, which are responsible for the epidemics in Japan and Korea, respectively ( Vandelle et al, 2020 ). Several T3Es secreted by the T3SS apparatus have been reported to be involved in pathogenicity in Psa3, such as HopZ5 ( Zhao et al, 2019a ), AvrE1, and HopR1 ( Jayaraman et al, 2020 ). In this study, we found that T3Es HopBB1-1 and HopBB1-2 were incomplete in Psa3 isolate G35, which showed attenuated HR-eliciting activity in N. benthamina leaves and moderate pathogenicity in host plants.…”

Section: Discussionmentioning

confidence: 99%

Genetic Causes of Non-pathogenic Pseudomonas syringae pv. actinidiae Isolates in Kiwifruit Orchards

Zhu

Zhi

et al. 2021

Front. Microbiol.

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Bacterial canker disease has become the largest threat to kiwifruit cultivation and production. A monomorphic subpopulation of Pseudomonas syringae pv. actinidiae biovar 3 (Psa3) is responsible for the pandemic worldwide. Diversity in pathogenicity has been found in the pandemic subpopulation and in other Psa3 subpopulations causing epidemics in China. However, the genetic bases have not yet been elucidated. In this study, 117 Psa3 isolates were identified by Psa- and Psa3-specific primers, and evaluated for pathogenicity. Three isolates G4, G40, and S2 are not pathogenic to kiwifruit and do not elicit hypersensitivity responses (HRs) in non-host Nicotiana benthamiana leaves. Two isolates, G25 and G35, exhibited attenuated HR-eliciting activity in non-host N. benthamiana, but they exhibited greatly and slightly reduced pathogenicity in host plants, respectively. The genomes of the five isolates were sequenced and compared with closely related isolates revealed by MLVA and whole-genome typing methods. The candidate genetic loci responsible for the changes in pathogenicity and HR elicitation, were further evaluated by allele replacement experiments. We found that the three non-pathogenic isolates were formed due to the independent, identical insertion events of ISPsy36 transposon in the hrpR gene, encoding a key regulator of type III secretion system (T3SS) and type III effectors (T3Es). In the symptomatic sample from which G4 was isolated, 27% HR negative isolates were detected. In isolate G25, transposon insertion of ISPsy32 at the non-coding sequence upstream of the hrpR gene was detected, similar to a previously reported low-virulent Psa3 strain M227. In isolate G35, we detected disruptions of T3Es hopBB1-1 and hopBB1-2, which induce HR in N. benthamiana leaves revealed by Agrobacterium tumefaciens infiltration. These phenotype-changed isolates were formed at low frequencies during the course of pathogen infection in host plants, supported by the binding assay of ISPsy32 and the non-coding DNA sequences upstream of the hrpR gene, the co-isolation of the virulent isolates belonging to the same MLVA clade, and the low levels of transcription of the transposon genes. Taken together, in terms of short-term field evolution, transposon insertions in the T3SS-related genes resulted in the formation of non-pathogenic and low-virulent Psa3 isolates.

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AvrE1 and HopR1 from Pseudomonas syringae pv. actinidiae are additively required for full virulence on kiwifruit

Cited by 32 publications

References 49 publications

Pseudomonas syringae pv. actinidiae Effector HopAU1 Interacts with Calcium-Sensing Receptor to Activate Plant Immunity

Pseudomonas syringae pv. actinidiae Effector HopAU1 Interacts with Calcium-Sensing Receptor to Activate Plant Immunity

Complete genome sequence of the kiwifruit bacterial canker pathogen Pseudomonas savastanoi strain MHT1

Genetic Causes of Non-pathogenic Pseudomonas syringae pv. actinidiae Isolates in Kiwifruit Orchards

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