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Pseudomonas syringae pv. actinidiae strain:ICMP 20586

ABSTRACT: Pseudomonas syringae pv. actinidiae ICMP 20586 Genome sequencing and assembly

PROVIDER: PRJNA339321 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR5003786_1.fastq.gz	Fastqsanger.gz
	SRR5003786_2.fastq.gz	Fastqsanger.gz
	SRR5003787_subreads.fastq.gz	Fastqsanger.gz

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Gene expression changes of Pseudomonas syringae pv. actinidiae biovar 6 in various culture conditions

Project description:Pseudomonas syringae pv. actinidiae biovar 6 (Psa6) is a causal agent of kiwifruit bacterial canker and is a unique plant pathogenic bacterium, producing two types of phytotoxins, coronatine and phaseolotoxin. We investigated the expression behavior of virulent genes of Psa6 under various culture conditions.

2020-05-02 | GSE149743 | GEO

Whole-transcriptome microarray analysis of Pseudomonas syringae pv. actinidiae CRAFRU 8.43 and Pseudomonas syringae pv. tomato DC3000 grown in apoplast-like conditions supplemented or not with kiwifruit or tomato extract

Project description:Purpose: The outcome of host–pathogen interactions is thought to reflect the offensive and defensive capabilities of both players. When plants interact with Pseudomonas syringae, several well-characterized virulence factors contribute to early bacterial pathogenicity, including the type III secretion system (T3SS), which must be activated by signals from the plant and environment to allow the secretion of virulence effectors. The manner in which these signals regulate T3SS activity is still unclear. Conlusion: the analysis revealed that the perception of plant signals from kiwifruit or tomato extracts anticipates T3SS expression in P. syringae pv. actinidiae compared to apoplast-like conditions

2022-08-25 | GSE211939 | GEO

Gene regulatory networks of kiwifruit response to Pseudomonas syringae pv. actinidiae

Project description:To study the responses of kiwifruit to Pseudomonas syringae pv. actinidiae, one-year-old potted seeding A. c. var. deliciosa cultivar ‘Jinkui’ and the pandemic Pseudomonas syringae pv. actinidiae bacterial strain JF8 (CCTCC AB2018305) were used for this study. This bacterial strain was originally isolated from A. c. var. chinensis cultivar ‘Jinfeng’ and further characterized . Plants were maintained in an aseptic room, with 95% of relative humidity, have natural light and no further fertilization after their receiving from the nursery. For inoculation, the P. s.pv. actinidiae strain was streaked on nutrient-sucrose agar (NSA) and incubated at 25 °C for 48-h. Ten microliters of a bacterial suspension (1-2×107cfu/mL) prepared in sterile 0.85 % w NaCl were inoculated in the plants chosen for investigation. The bacterial suspension was sprayed to entirety tree. In parallel, control plants were treated in the same way with sterile 0.85 % w NaCl solution. The inoculated and control plants were randomly distributed in the room at 15 ± 3 °C. 24-h after inoculation, ‘Jinkui’ leaves were sampled from the infected and control plants for further analyses. Each sample consisted of the leaves of one tree. Three biological replicates were used for each line.

2021-11-10 | PXD014787 | Pride

Whole-transcriptome microarray analysis of different biovars of Pseudomonas syringae pv. actinidiae grown in rich medium or apoplast-like conditions

Project description:Purpose: Pseudomonas syringae pv. actinidiae (Psa) is a phytopathogen that causes devastating bacterial canker in kiwifruit. Among five biovars defined by genetic, biochemical and virulence traits, Psa3 is the most aggressive and is responsible for the most recent reported outbreaks, but the molecular basis of its heightened virulence is unclear. A custom P. syringae multi-strain whole-genome microarray platform, encompassing biovars Psa1, Psa2 and Psa3 and the well-established model P. syringae pv. tomato, was used to analyse early bacterial responses to an apoplast-like minimal medium. Conlusion: this work highlighted that diverse early responses to the host apoplast, even among bacteria belonging to the same pathovar, can lead to different virulence strategies and may explain the differing outcomes of infections.

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A low temperature-sensitive regulator that enhances virulence in the kiwifruit canker pathogen Pseudomonas syringae pv. actinidiae

Project description:Pseudomonas syringae pv. actinidiae (Psa) is responsible for causing kiwifruit canker disease, which severely impacts on the global kiwifruit industry, leading to substantial economic losses. Cooler environmental temperatures (below 20℃) are known to favor the outbreak of this bacterial disease in the field. However, the specific mechanisms that enable Psa to adapt and thrive in such conditions have remained elusive. In this study, we discovered that the gene RS16350, encoding a heat shock protein, positively regulates pathogenicity in kiwifruit leaves at low temperature (16℃), but not at room temperature (28℃). Delving into the mechanics, we found that RS16350 directly interacts with HrpL, an RpoN-dependent RNA polymerase sigma factor that serves as a master regulator of the type III secretion system (T3SS) in Psa. This RS16350-HrpL interaction enhances HrpL’s binding affinity to hrp-box, which in turn elevates the expression of downstream T3SS genes, thereby boosting virulence. Consequently, we have designated RS16350 as TspR (temperature sensitive and pathogenic regulator). Our findings shed light on how a kiwi pathogen enhances its virulence in response to low temperatures, paving the way for the development of innovative strategies to combat kiwifruit canker disease.

2025-06-16 | GSE283068 | GEO

RetS-Mediated Environmental Sensing Coordinates TetR-Dependent Regulation of Type III Secretion System and Virulence in Pseudomonas syringae pv. actinidiae

Project description:Kiwifruit bacterial canker, caused by Pseudomonas syringae pv. actinidiae (Psa), is an emerging global concern in kiwifruit production. Successful Psa infection in kiwifruit relies on the type III secretion system (T3SS), which is governed by the HrpR/S-HrpL regulatory pathway. However, the mechanisms by which certain transcriptional factors regulate this pathway remain poorly understood. In this study, we identified the TetR/AcrR family transcription factors C_22735 (tetR1) and C_04700 (hybrid histidine kinase; retS) in the P. syringae pv. actinidiae (biovar 3) strain S26 using transposon libraries and a DNA pull-down strategy. Both the mutant strains tetR1 and retS exhibited significantly reduced pathogenicity in kiwifruit leaf discs and a diminished ability to induce hrpRS, hrpL, and hrpA expression in vitro and showed a reduced hypersensitive response in Nicotiana benthamiana. Moreover, transcriptomic studies showed a considerable overlap in down-regulated genes between the tetR1 and two-component system (TCS) retS mutant, highlighting the intertwined regulatory roles of both genes. This overlap suggests a tightly coordinated regulatory system, where tetR1 serves as the response regulator of the hybrid histidine kinase retS to regulate T3SS and virulence. The electrophoretic mobility shift assays, and luciferase-based promoter activity detection further revealed that TetR1 positively regulates the T3SS by directly binding to the promoter regions of hrpR/S and hrpL. This study identifies the tetR1 gene as the first TetR-family transcription factor directly linking the hybrid TCS retS to HrpR/S-HrpL -mediated T3SS regulatory pathway activation in Psa for regulation.

2025-01-31 | GSE286487 | GEO

Whole-transcriptome microarray analysis of Pseudomonas syringae pv. actinidiae (Psa) treated with Gunpowder green tea extract (EGCG 0.4 mg/ml)

Project description:Purpose: Microarray technologies provide a unique opportunity to deeply investigate bacterial molecular responses to treatments. Pseudomonas syringae pv. actinidiae (Psa) is the causal agent of the bacterial canker of kiwifruit causing severe economic losses worldwide. At present, integrated control strategies include chemical treatments with copper-based products and preventive measures but the high virulence and fast spreading of the bacterium are hardly controlled by such measures, and especially copper use is questioned because of the possible appearance of copper resistant bacterial strains. The present project aims at the identification of Psa responses to green tea treatment (Gunpowder variety) at sub-lethal concentration (0.4 mg/ml). Methods: Psa cells were cultured in liquid KB (controls) or in KB supplemented with Gunpowder tea (Gunpowder-trateted) at 0.4 mg/ml EGCG for 24 h at 28°C. The microarray experiments on Gunpowder treated or untreated samples in biological triplicate resulted in 6 samples to be analyzed. Conclusions: This work identified important molecular mechanisms involved in Psa responses upon Gunpowder green tea treatment.

2019-09-23 | GSE137806 | GEO

Pseudomonas syringae pv. actinidiae

Project description:Origin and evolution of the kiwifruit pathogen Pseudomonas syringae pv. actinidiae

| PRJNA359702 | ENA

Pseudomonas syringae pv. actinidiae

Project description:Pseudomonas syringae pv. actinidiae isolates from kiwifruit buds

| PRJNA826138 | ENA

Novel insights into the genetic basis and proteotranscriptomic elucidation of virulence attenuation in Pseudomonas syringae pv. actinidiae variants

Project description:Pseudomonas syringae pv. actinidiae (Psa) is the causal agent of kiwifruit bacterial canker, but the factors affecting its pathogenicity in natural settings remain poorly explored. In this study, we isolated two Psa strains, G126 and G282 from infected kiwifruit orchards in Guizhou Province of China. Both isolates, categorized as Psa-biovar 3, were confirmed through Psa3-specific primers and phylogenomic analysis. Pathogenicity assays on kiwifruit cultivar ‘Hongyang’ leaves and branches showed significantly reduced numbers of necrotic spots and reduced lesions sizes upon infection with G282 compared to the G1 positive control strain, while G126 showed nonpathogenic phenotype. Additionally, both strains failed to induce a hypersensitive response in nonhost Nicotiana tabacum plants, and exhibited significantly reduced promoter activity of the hrpR/S, hrpL, and hrpA genes, which are crucial for the type III secretion system (T3SS). Genomic sequencing revealed that the T3SS of G126 was defective due to a single-nucleotide polymorphism in the hrpR gene, while G282 was entirely deficient in the type VI secretion system (T6SS), which potentially regulates the expression of T3SS genes. Transcriptomic analysis showed widespread alterations in key aspects of the secretion system, protein transport, and signal transduction, further supporting the phenotype characteristics exhibited by the strains. This study enhances our understanding of the genetic basis of nonpathogenic and partially pathogenic Psa isolates, highlighting the functional interdependencies between T3SS and T6SS.

2025-01-31 | GSE286024 | GEO

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