Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Complete DNA Sequence of Pseudomonas syringae pv. actinidiae, the Causal Agent of Kiwifruit Canker Disease.

ABSTRACT: Pseudomonas syringae pv. actinidiae is the causal agent of bacterial canker of kiwifruit, a disease that has rapidly spread worldwide. We have fully sequenced and assembled the chromosomal and plasmid DNA from P. syringae pv. actinidiae ICMP 18884 using the PacBio RS II platform.

SUBMITTER: Templeton MD

PROVIDER: S-EPMC4574371 | biostudies-literature | 2015 Sep

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Complete DNA Sequence of Pseudomonas syringae pv. actinidiae, the Causal Agent of Kiwifruit Canker Disease.

Templeton Matthew D MD Warren Benjamin A BA Andersen Mark T MT Rikkerink Erik H A EH Fineran Peter C PC

Genome announcements 20150917 5

Pseudomonas syringae pv. actinidiae is the causal agent of bacterial canker of kiwifruit, a disease that has rapidly spread worldwide. We have fully sequenced and assembled the chromosomal and plasmid DNA from P. syringae pv. actinidiae ICMP 18884 using the PacBio RS II platform. ...[more]

PMID: 26383666

Similar Datasets

Genome analysis of the kiwifruit canker pathogen Pseudomonas syringae pv. actinidiae biovar 5.

Project description:Pseudomonas syringae pv. actinidiae (Psa) is a destructive pathogen of kiwifruit bacterial canker disease, causing severe economic losses to kiwifruit industry worldwide. Biovar 5 is the most recently reported biovar of Psa, and is found in only a local area of Japan at present. There is not much information of genetic characteristics of biovar 5. Thus, the genome of biovar 5 was sequenced and analyzed to clarify its detailed genetic characteristics. Here, the genomes of strain MAFF 212056 and MAFF 212061 of biovar 5 were estimated to be about 6.3 Mbp and 6.5 Mbp, respectively, and their phylogenetic positions were proved to be near that of biovar 2 in the phylogenetic tree. However, it was confirmed that biovar 5 had neither the coronatine biosynthetic genes conserved in biovar 2, its phylogenetic neighbor, nor the phaseolotoxin biosynthetic genes conserved in biovar 1, Japanese native pathogen. In addition, 45 genes of type III secreted effectors were identified in biovar 5 genomes, showing that their composition is different from that in the other biovars. Moreover, some biovar 5-specific regions were identified. Then, biovar 5-specific PCR primers for targeting these regions were designed, and proved to be applicable for detecting biovar 5 specifically.

| S-EPMC4759546 | biostudies-literature

Identification of bacteriophages for biocontrol of the kiwifruit canker phytopathogen Pseudomonas syringae pv. actinidiae.

Project description:Pseudomonas syringae pv. actinidiae is a reemerging pathogen which causes bacterial canker of kiwifruit (Actinidia sp.). Since 2008, a global outbreak of P. syringae pv. actinidiae has occurred, and in 2010 this pathogen was detected in New Zealand. The economic impact and the development of resistance in P. syringae pv. actinidiae and other pathovars against antibiotics and copper sprays have led to a search for alternative management strategies. We isolated 275 phages, 258 of which were active against P. syringae pv. actinidiae. Extensive host range testing on P. syringae pv. actinidiae, other pseudomonads, and bacteria isolated from kiwifruit orchards showed that most phages have a narrow host range. Twenty-four were analyzed by electron microscopy, pulse-field gel electrophoresis, and restriction digestion. Their suitability for biocontrol was tested by assessing stability and the absence of lysogeny and transduction. A detailed host range was performed, phage-resistant bacteria were isolated, and resistance to other phages was examined. The phages belonged to the Caudovirales and were analyzed based on morphology and genome size, which showed them to be representatives of Myoviridae, Podoviridae, and Siphoviridae. Twenty-one Myoviridae members have similar morphologies and genome sizes yet differ in restriction patterns, host range, and resistance, indicating a closely related group. Nine of these Myoviridae members were sequenced, and each was unique. The most closely related sequenced phages were a group infecting Pseudomonas aeruginosa and characterized by phages JG004 and PAK_P1. In summary, this study reports the isolation and characterization of P. syringae pv. actinidiae phages and provides a framework for the intelligent formulation of phage biocontrol agents against kiwifruit bacterial canker.

| S-EPMC3993152 | biostudies-literature

Pathways of flower infection and pollen-mediated dispersion of Pseudomonas syringae pv. actinidiae, the causal agent of kiwifruit bacterial canker.

Project description:Flowers can provide a protected and nutrient-rich environment to the epiphytic microflora, thus representing a sensible entry point for pathogens such as Pseudomonas syringae pv. actinidiae (Psa). This bacterium can colonize both male and female Actinidia flowers, causing flower browning and fall, and systemic invasion of the host plant, eventually leading to its death. However, the process of flower colonization and penetration into the host tissues has not yet been fully elucidated. In addition, the presence of Psa in the pollen from infected flowers, and the role of pollination in the spread of Psa requires confirmation. The present study employed a Psa strain constitutively expressing the fluorescent GFPuv protein, to visualize in vivo flower colonization. Microscopy observations were performed by means of confocal laser scanning and wide-field fluorescent microscopy, and were coupled with the study of Psa population dynamics by quantitative PCR (q-PCR). The pathogen was shown to colonize stigmata, move along the stylar furrow, and penetrate the receptacles via the style or nectarhodes. Once the receptacle was invaded, the pathogen migrated along the flower pedicel and became systemic. Psa was also able to colonize the anthers epiphytically and endophytically. Infected male flowers produced contaminated pollen, which could transmit Psa to healthy plants. Finally, pollinators (Apis mellifera and Bombus terrestris) were studied in natural conditions, showing that, although they can be contaminated with Psa, the pathogen's transmission via pollinators is contrasted by its short survival in the hive.

| S-EPMC6210195 | biostudies-literature

Complete Genome Sequence of the Kiwifruit Pathogen Pseudomonas syringae pv. actinidiae Biovar 5, Originating from Japan.

Project description:We present the first complete genome sequence of a copper-resistant biovar 5 strain of a bacterial pathogen of kiwifruit, Pseudomonas syringae pv. actinidiae. Comparison with the genome sequence of a copper-sensitive biovar 5 isolate indicates that copper resistance is encoded on a plasmid.

| S-EPMC5730677 | biostudies-literature

dCas9-BE3 and dCas12a-BE3 Systems Mediated Base Editing in Kiwifruit Canker Causal Agent Pseudomonas syringae pv. actinidiae.

Project description:Pseudomonas syringae pv. actinidiae (Psa) causes bacterial canker of kiwifruit with heavy economic losses. However, little is known about the pathogenic genes of Psa. CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats)/Cas-mediated genome editing technology has dramatically facilitated the characterization of gene function in various organisms. However, CRISPR genome editing could not be efficiently employed in Psa due to lacking homologous recombination repair. The base editor (BE) system, which depends on CRISPR/Cas, directly induces single nucleoside C to T without homology recombination repair. Here, we used dCas9-BE3 and dCas12a-BE3 systems to create substitutions of C to T and to convert CAG/CAA/CGA codons to stop codons (TAG/TAA/TGA) in Psa. The dCas9-BE3 system-induced single C-to-T conversion frequency of 3 to 10 base positions ranged from 0% to 100%, with a mean of 77%. The dCas12a-BE3 system-induced single C-to-T conversion frequency of 8 to 14 base positions in the spacer region ranged from 0% to 100%, with a mean of 76%. In addition, a relatively saturated Psa gene knockout system covering more than 95% of genes was developed based on dCas9-BE3 and dCas12a-BE3, which could knock out two or three genes at the same time in the Psa genome. We also found that hopF2 and hopAO2 were involved in the Psa virulence of kiwifruit. The HopF2 effector can potentially interact with proteins such as RIN, MKK5, and BAK1, while the HopAO2 effector can potentially interact with the EFR protein to reduce the host's immune response. In conclusion, for the first time, we established a PSA.AH.01 gene knockout library that may promote research on elucidating the gene function and pathogenesis of Psa.

| S-EPMC10003707 | biostudies-literature

Genome, Proteome and Structure of a T7-Like Bacteriophage of the Kiwifruit Canker Phytopathogen Pseudomonas syringae pv. actinidiae.

Project description:Pseudomonas syringae pv. actinidiae is an economically significant pathogen responsible for severe bacterial canker of kiwifruit (Actinidia sp.). Bacteriophages infecting this phytopathogen have potential as biocontrol agents as part of an integrated approach to the management of bacterial canker, and for use as molecular tools to study this bacterium. A variety of bacteriophages were previously isolated that infect P. syringae pv. actinidiae, and their basic properties were characterized to provide a framework for formulation of these phages as biocontrol agents. Here, we have examined in more detail φPsa17, a phage with the capacity to infect a broad range of P. syringae pv. actinidiae strains and the only member of the Podoviridae in this collection. Particle morphology was visualized using cryo-electron microscopy, the genome was sequenced, and its structural proteins were analysed using shotgun proteomics. These studies demonstrated that φPsa17 has a 40,525 bp genome, is a member of the T7likevirus genus and is closely related to the pseudomonad phages φPSA2 and gh-1. Eleven structural proteins (one scaffolding) were detected by proteomics and φPsa17 has a capsid of approximately 60 nm in diameter. No genes indicative of a lysogenic lifecycle were identified, suggesting the phage is obligately lytic. These features indicate that φPsa17 may be suitable for formulation as a biocontrol agent of P. syringae pv. actinidiae.

| S-EPMC4517105 | biostudies-literature

Genome Sequence of a Jumbo Bacteriophage That Infects the Kiwifruit Phytopathogen Pseudomonas syringae pv. actinidiae.

Project description:Bacteriophage ϕPsa21 is a potential biocontrol agent that infects the kiwifruit phytopathogen Pseudomonas syringae pv. actinidiae. ϕPsa21 is a "jumbo" phage with a genome of ∼305 kb. Here, we present the genome sequence of ϕPsa21 and discuss potential genes indicative of the formation of nucleoid structures during viral replication.

| S-EPMC6544186 | 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

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.

| S-EPMC7645661 | biostudies-literature

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data