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Evaluation of the Abilities of Three Kinds of Copper-Based Nanoparticles to Control Kiwifruit Bacterial Canker.

ABSTRACT: Kiwifruit bacterial canker caused by Pseudomonas syringae pv. actinidiae reduces kiwifruit crop yield and quality, leading to economic losses. Unfortunately, few agents for its control are available. We prepared three kinds of copper-based nanoparticles and applied them to control kiwifruit bacterial canker. The successful synthesis of Cu(OH)₂ nanowires, Cu₃(PO₄)₂ nanosheets, and Cu₄(OH)₆Cl₂ nanoparticles were confirmed by transmission and scanning electron microscopy, energy dispersive spectroscopy, X-ray diffraction analysis, and X-ray photoelectron spectroscopy. The minimum bactericidal concentrations (MBCs) of the three nanoparticles were 1.56 μg/mL, which exceeded that of the commercial agent thiodiazole copper (MBC > 100 μg/mL). The imaging results indicate that the nanoparticles could interact with bacterial surfaces and kill bacteria by inducing reactive oxygen species' accumulation and disrupting cell walls. The protective activities of Cu(OH)₂ nanowires and Cu₃(PO₄)₂ nanosheets were 59.8% and 63.2%, respectively, similar to thiodiazole copper (64.4%) and better than the Cu₄(OH)₆Cl₂ nanoparticles (40.2%). The therapeutic activity of Cu₄(OH)₆Cl₂ nanoparticles (67.1%) bested that of Cu(OH)₂ nanowires (43.9%), Cu₃(PO₄)₂ nanosheets (56.1%), and thiodiazole copper (53.7%). Their therapeutic and protective activities for control of kiwifruit bacterial canker differed in vivo, which was related to their sizes and morphologies. This study suggests these copper-based nanoparticles as alternatives to conventional bactericides for controlling kiwifruit diseases.

SUBMITTER: Ren G

PROVIDER: S-EPMC9312301 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Occurrence and Epidemics of Bacterial Canker of Kiwifruit in Korea.

Project description:Bacterial canker is the largest limiting factor in the cultivation and production of kiwifruit worldwide. Typical symptoms comprise necrotic spots on leaves, canker and dieback on canes and trunks, twig wilting, and blossom necrosis. Pseudomonas syringae pv. actinidiae (Psa), which is the causal agent of kiwifruit bacterial canker, is divided into four biovars based on multilocus sequence analysis of different genes, additional PCR testing of pathogenic genes (argKtox cluster, cfl, and various effector genes), and biochemical and physiological characterization. Bacterial canker caused by Psa biovar 2 designated Psa2 was detected for the first time on the green-fleshed kiwifruit cultivar Hayward in 1988 and the yellow-fleshed kiwifruit cultivar Hort16A in 2006 in Korea. Psa biovar 3 designated Psa3, responsible for the current global pandemics of kiwifruit bacterial canker, began to appear in Korea in 2011 and caused tremendous economic losses by destroying many vines or orchards of yellow-fleshed kiwifruit cultivars in one or several growing seasons. Bacterial canker epidemics caused by both Psa2 and Psa3 are prevalent in Korea in recent years. In this review, we summarize the symptomatology, etiology, disease cycle, diagnosis, and epidemiology of kiwifruit bacterial canker in Korea.

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Characterization of Antibacterial Strains against Kiwifruit Bacterial Canker Pathogen.

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| S-EPMC6724088 | biostudies-other

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Project description:Research studies have recently focused on circle RNAs (circRNAs) in relation to their regulatory functions in animals. However, the systematic identification of circRNAs in plants, especially non-model plants, is limited. In addition, raw report on the prediction of the potential role of circRNAs in plant response to pathogen invasion is currently available. We conducted the systematic identification of circRNAs from four materials originating from three species belonging to genus Actinidia under different situations using ribosomal RNA (rRNA) depleted RNA-Seq data. A total of 3,582 circRNAs were identified in Actinidia, of which 64.01, 21.44, and 14.55% were intergenic circRNAs, exonic circRNAs, and intronic circRNAs, respectively. Tissue-specific expression of circRNAs was observed in kiwifruit, and a species-specific response was detected when infected with Pseudomonas syringae pv. actinidiae (Psa), which is the causative agent of kiwifruit bacterial canker disease. Furthermore, we found that both exonic and intronic circRNAs were significantly positively correlated to parent protein-coding genes, and intronic circRNAs are a class of highly remarkable regulators the parent genes comparing to that of exonic circRNAs. Expression and weighted gene co-expression network analysis (WGCNA) identified a set of circRNAs that were closely associated with plant defense response. The findings of the presents study suggest that circRNAs exhibit tissue- and species-specific expression, as well as play an important role in plant immune response.

| S-EPMC5366334 | biostudies-literature

Draft Genome Sequences of Nine Japanese Strains of the Kiwifruit Bacterial Canker Pathogen Pseudomonas syringae pv. actinidiae Biovar 3.

Project description:Pseudomonas syringae pv. actinidiae is the pathogen that causes kiwifruit bacterial canker and is categorized into several groups (biovars). In Japan, biovar 3, known as the pandemic group, was first discovered in 2014. Here, we sequenced the genomes of nine Japanese biovar 3 strains.

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Pseudomonas syringae pv. actinidiae from recent outbreaks of kiwifruit bacterial canker belong to different clones that originated in China.

Project description:A recently emerged plant disease, bacterial canker of kiwifruit (Actinidia deliciosa and A. chinensis), is caused by Pseudomonas syringae pv. actinidiae (PSA). The disease was first reported in China and Japan in the 1980s. A severe outbreak of PSA began in Italy in 2008 and has spread to other European countries. PSA was found in both New Zealand and Chile in 2010. To study the evolution of the pathogen and analyse the transmission of PSA between countries, genomes of strains from China and Japan (where the genus Actinidia is endemic), Italy, New Zealand and Chile were sequenced. The genomes of PSA strains are very similar. However, all strains from New Zealand share several single nucleotide polymorphisms (SNPs) that distinguish them from all other PSA strains. Similarly, all the PSA strains from the 2008 Italian outbreak form a distinct clonal group and those from Chile form a third group. In addition to the rare SNPs present in the core genomes, there is abundant genetic diversity in a genomic island that is part of the accessory genome. The island from several Chinese strains is almost identical to the island present in the New Zealand strains. The island from a different Chinese strain is identical to the island present in the strains from the recent Italian outbreak. The Chilean strains of PSA carry a third variant of this island. These genomic islands are integrative conjugative elements (ICEs). Sequencing of these ICEs provides evidence of three recent horizontal transmissions of ICE from other strains of Pseudomonas syringae to PSA. The analyses of the core genome SNPs and the ICEs, combined with disease history, all support the hypothesis of an independent Chinese origin for both the Italian and the New Zealand outbreaks and suggest the Chilean strains also originate from China.

| S-EPMC3583860 | biostudies-literature

Pseudomonas syringae pv. actinidiae (PSA) isolates from recent bacterial canker of kiwifruit outbreaks belong to the same genetic lineage.

Project description:Intercontinental spread of emerging plant diseases is one of the most serious threats to world agriculture. One emerging disease is bacterial canker of kiwi fruit (Actinidia deliciosa and A. chinensis) caused by Pseudomonas syringae pv. actinidiae (PSA). The disease first occurred in China and Japan in the 1980s and in Korea and Italy in the 1990s. A more severe form of the disease broke out in Italy in 2008 and in additional countries in 2010 and 2011 threatening the viability of the global kiwi fruit industry. To start investigating the source and routes of international transmission of PSA, genomes of strains from China (the country of origin of the genus Actinidia), Japan, Korea, Italy and Portugal have been sequenced. Strains from China, Italy, and Portugal have been found to belong to the same clonal lineage with only 6 single nucleotide polymorphisms (SNPs) in 3,453,192 bp and one genomic island distinguishing the Chinese strains from the European strains. Not more than two SNPs distinguish each of the Italian and Portuguese strains from each other. The Japanese and Korean strains belong to a separate genetic lineage as previously reported. Analysis of additional European isolates and of New Zealand isolates exploiting genome-derived markers showed that these strains belong to the same lineage as the Italian and Chinese strains. Interestingly, the analyzed New Zealand strains are identical to European strains at the tested SNP loci but test positive for the genomic island present in the sequenced Chinese strains and negative for the genomic island present in the European strains. Results are interpreted in regard to the possible direction of movement of the pathogen between countries and suggest a possible Chinese origin of the European and New Zealand outbreaks.

| S-EPMC3348921 | biostudies-literature

Multiple quantitative trait loci contribute to resistance to bacterial canker incited by Pseudomonas syringae pv. actinidiae in kiwifruit (Actinidia chinensis).

Project description:Pseudomonas syringae pv. actinidiae (Psa) biovar 3, a virulent, canker-inducing pathogen is an economic threat to the kiwifruit (Actinidia spp.) industry worldwide. The commercially grown diploid (2×) A. chinensis var. chinensis is more susceptible to Psa than tetraploid and hexaploid kiwifruit. However information on the genetic loci modulating Psa resistance in kiwifruit is not available. Here we report mapping of quantitative trait loci (QTLs) regulating resistance to Psa in a diploid kiwifruit population, derived from a cross between an elite Psa-susceptible 'Hort16A' and a resistant male breeding parent P1. Using high-density genetic maps and intensive phenotyping, we identified a single QTL for Psa resistance on Linkage Group (LG) 27 of 'Hort16A' revealing 16-19% phenotypic variance and candidate alleles for susceptibility and resistance at this loci. In addition, six minor QTLs were identified in P1 on distinct LGs, exerting 4-9% variance. Resistance in the F1 population is improved by additive effects from 'Hort16A' and P1 QTLs providing evidence that divergent genetic pathways interact to combat the virulent Psa strain. Two different bioassays further identified new QTLs for tissue-specific responses to Psa. The genetic marker at LG27 QTL was further verified for association with Psa resistance in diploid Actinidia chinensis populations. Transcriptome analysis of Psa-resistant and susceptible genotypes in field revealed hallmarks of basal defense and provided candidate RNA-biomarkers for screening for Psa resistance in greenhouse conditions.

| S-EPMC6804790 | biostudies-literature

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