Novel insights into the genetic basis and proteotranscriptomic elucidation of virulence attenuation in Pseudomonas syringae pv. actinidiae variants
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PROVIDER: PRJNA1207504 | ENA |
REPOSITORIES: ENA
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Project description:Pseudomonas syringae pv. actinidiae (Psa) is the potential cause of Kiwifruit Bacterial Canker (KBC) but the factors affecting its pathogenicity in natural setting is less elaborated. Here, we isolated two Psa3 strains, G126 and G282, from Guizhou province`s kiwifruit orchards suffering from KBC disease. Both isolates belonging to Psa-biovar 3 were verified by Psa3-specific primers. Compared to Psa3-G1 positive control strain, G282 exhibited significant reduction of necrotic spots and lesion density during pathogenicity assays on kiwifruit leaf discs and branches, while G126 was unable to show any disease phenotype. Similarly, no induction of hypersensitive response in tobacco plants as well as significantly reduced promoter’s activities of hrpA, hrpR/S/L of type III secretion system (T3SS) cascade suggested that both strains are defective in functional T3SS-dependent phenotypes. Genomic sequencing of these strains revealed that T3SS pathway of G126 was defective due to a single-nucleotide polymorphism variation in hrpR gene, while G282 was entirely deprived of T6SS to potentially transmit T3SS effectors. In addition, transcriptomic analysis of GO and KEGG pathways revealed several key aspects related to the secretion system, protein transport and signal transduction being widely affected. This study advances our understanding to the genetic basis of these non-pathogenic and partial pathogenic isolates, and the functional interdependencies between secretion systems (T3SS, T6SS) and metabolic or motility-related pathways, showcasing how genetic mutations lead to widespread physiological changes will provide insights into virulence evolution, the identification of pathogenic determinants, and the development of biocontrol strategies against Psa.
2025-01-31 | GSE286024 | GEO
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
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
Project description:In some patients, Escherichia coli strains establish significant bacteriuria without causing symptoms of urinary tract infection (UTI). These asymptomatic-bacteriuria (ABU) strains have been shown to express fewer virulence factors than the uropathogenic E. coli (UPEC) strains that cause severe, symptomatic UTI. Paradoxically, ABU strains carry many typical UPEC virulence genes, and the molecular basis of their low virulence therefore remains unclear. This study examined whether ABU strains might evolve from UPEC by genome loss and virulence gene attenuation. The presence of conserved E. coli K-12 genes was examined using an E. coli K-12 strain MG1655-specific DNA array and the distribution of UPEC virulence-related genes was examined with the E. coli pathoarray. Two groups of strains could be distinguished. Several ABU strains were shown by multilocus sequence typing and by comparative genomic analyses to be related to UPEC but to have smaller genome sizes. There were significant alterations in essential virulence genes, including reductive evolution by point mutations, DNA rearrangements, and deletions. Other strains were unrelated to UPEC and lacked most of the virulence-associated genes. The results suggest that some ABU strains arise from virulent strains by attenuation of virulence genes while others are nonvirulent and resemble commensal strains. We propose that virulence attenuation might constitute a general mechanism for mucosal pathogens to evolve toward commensalism.
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Project description:Pectobacterium actinidiae Genome sequencing
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Project description:A ChIP-seq assay was performed to identify the regulons of an ompR-like transcription factor (gene name: 13375, GenBank: AYL80818.1) in Pseudomonas syringae pv. actinidiae. An 13375-overexpressing mutant G1-OE13375, which constitutively express C-terminally Myc-tagged ompR-like gene in the 13375-deletion mutant G1Δ13375, was used in this study. The bacterial cells were cultured either in nutrition-rich KB medium or hrp-derepressing medium (HDM) at 25 C for 24 hours. A PierceTM Magnetic ChIP Kit (Cat. #: 26157, Thermo Fisher Scientific) and a ChIP-grade Myc-Tag Monoclonal Antibody (Myc.A7, Cat. #: MA121316, Thermo Fisher Scientific) were used for sample pretreatment and immunoprecipitation.
2022-12-13 | GSE220275 | GEO
Project description:Attenuated viruses have numerous applications, in particular in the context of live viral vaccines. However, purposefully designing attenuated viruses remains challenging, in particular if the attenuation is meant to be resistant to rapid evolutionary recovery. Here we develop and analyze a new attenuation method, promoter ablation, using an established viral model, bacteriophage T7. Ablating promoters of the two most highly expressed T7 proteins (scaffold and capsid) led to major reductions in transcript abundance of the affected genes, with the effect of the double knockout approximately additive of the effects of single knockouts. Fitness reduction was moderate and also approximately additive; fitness recovery on extended adaptation was partial and did not restore the promoters. The fitness effect of promoter knockouts combined with a previously tested codon deoptimization of the capsid gene was less than additive, as anticipated from their competing mechanisms of action. In one design, the engineering created an unintended consequence that led to further attenuation, the effect of which was studied and understood in hindsight. Overall, the mechanisms and effects of genome engineering on attenuation behaved in a predictable manner. Therefore, this work suggests that the rational design of viral attenuation methods is becoming feasible.
2018-06-07 | GSE115396 | GEO
Project description:Combinitorial Approaches to Viral Attenuation
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Project description:Systematic elucidation of genetic mechanisms underlying cholesterol uptake
2023-04-21 | GSE229650 | GEO