Nucleotide Sequences, Genetic Organization, and Distribution of pEU30 and pEL60 from
            <i>Erwinia amylovora</i>

Foster, Gayle C.; McGhee, Gayle C.; Jones, Alan L.; Sundin, George W.

doi:10.1128/aem.70.12.7539-7544.2004

Cited by 52 publications

(58 citation statements)

References 22 publications

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“…Plasmids appear to be a major factor influencing the pan-genome of E. amylovora. However, although several plasmids of different sizes have been detected in isolates of this species (Chiou and Jones 1991;Foster et al 2004;Laurent et al 1989;McGhee et al 2002;Steinberger et al 1990), the knowledge on this extra-chromosomal material is limited to few strains and plasmids.…”

Section: Erwinia Amylovora Genomicsmentioning

confidence: 99%

Genomics and current genetic understanding of Erwinia amylovora and the fire blight antagonist Pantoea vagans

Kamber

Smits

Rezzonico

et al. 2011

Trees

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The bacterial plant pathogen Erwinia amylovora causes fire blight, a major disease threat to pome fruit production worldwide with further impact on a wide-range of Rosaceae species. Important factors contributing to the development of the disease were discovered in the last decades. Comparative genomics of the genera Erwinia and Pantoea is coming into focus with the recent availability of complete genome sequences. Insights from comparative genomics now position us to answer fundamental questions regarding the evolution of E. amylovora as a successful pathogen and the critical elements for biocontrol activity of Pantoea spp. This trove of new data promises to reveal novel determinants and to understand interactive pathways for virulence, host range and ecological fitness. The ultimate aim is now to apply genomics and identify the pathogen Achilles heels and antagonist mechanisms of action as targets for designing innovative control strategies for fire blight.

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Section: Erwinia Amylovora Genomicsmentioning

confidence: 99%

Genomics and current genetic understanding of Erwinia amylovora and the fire blight antagonist Pantoea vagans

Kamber

Smits

Rezzonico

et al. 2011

Trees

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“…The second cycle of PSIBLAST identified another group of DsbC H homologues from other H-like plasmids (E values ϭ 2e Ϫ14 to 3e Ϫ23 ), establishing homology to H-like HtdT proteins (E value ϭ 4e Ϫ4 ) and the chromosomally encoded E. coli DsbG (E value ϭ 5e Ϫ16 ) ( Table 3). Subsequent cycles of PSIBLAST using a PSSM inclusion threshold of 0.001 revealed homology to the TrbB proteins encoded by the IncI plasmids R64 (25), ColIb-P9 (60), pEL60 (23), and pCTX-M3 (accession number, NC_004464) (E values ϭ 4e Ϫ6 to 5e Ϫ15 ). The naming of R64 TrbB and F TrbB was coincidental; discerning the relationship between these two proteins required many iterations of PSIBLAST, suggesting that they are, at best, distantly related.…”

Section: F-and H-like Transfer Regions Encode Putative Thiol-disulfidmentioning

confidence: 99%

F-Like Type IV Secretion Systems Encode Proteins with Thioredoxin Folds That Are Putative DsbC Homologues

Elton

Holland²,

Frost³

et al. 2005

J Bacteriol

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F and R27 are conjugative plasmids of enteric bacteria belonging to the IncF and IncHI1 plasmid incompatibility groups, respectively. Based on sequence analysis, two genes of the F transfer region, traF and trbB, and three genes of the R27 transfer region, trhF, dsbC, and htdT, are predicted to encode periplasmic proteins containing a C-terminal thioredoxin fold. The C-X-X-C active-site motif of thioredoxins is present in all of these proteins except TraF F . Escherichia coli carrying a dsbA mutation, which is deficient in disulfide bond formation, cannot synthesize pili and exhibits hypersensitivity to dithiothreitol (DTT) as monitored by mating ability. Overproduction of the E. coli disulfide bond isomerase DsbC, TrbB F , DsbC R27 , or HtdT R27 , but not TraF F or TrhF R27 , reverses this hypersensitivity to DTT. Site-directed mutagenesis established that the C-X-X-C motif was necessary for this activity. Secretion into the periplasm of the C-terminal regions of TrbB F and DsbC R27 , containing putative thioredoxin folds, but not TrhF R27 , partially complemented the host dsbA mutation. A trbB F deletion mutant showed a 10-fold-lower mating efficiency in an E. coli dsbC null strain but had no phenotype in wild-type E. coli, suggesting redundancy in function between TrbB F and E. coli DsbC. Our results indicate that TrbB F , DsbC R27 , and HtdT R27 are putative disulfide bond isomerases for their respective transfer systems. TraF F is essential for conjugation but appears to have a function other than disulfide bond chemistry.

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“…E. piriflorinigrans strains CFBP 5888 T and CFBP 5887 (Table 1) were used to conduct four independent stability assays according to the procedure of Foster et al (19). A single colony of each bacterial strain was incubated in 4.5 ml of Luria-Bertani (LB) broth medium (20) at 26°C for 24 h under shaking at 220 rpm (Barnstead LabLine MaxQ 4000 shaker).…”

Section: Methodsmentioning

confidence: 99%

Conventional and Real-Time PCRs for Detection of Erwinia piriflorinigrans Allow Its Distinction from the Fire Blight Pathogen, Erwinia amylovora

Barbé

Bertolini

Roselló

et al. 2014

Appl Environ Microbiol

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bErwinia piriflorinigrans is a new pathogenic species of the bacterial genus Erwinia that has been described recently in Spain. Accurate detection and identification of E. piriflorinigrans are challenging because its symptoms on pear blossoms are similar to those caused by Erwinia amylovora, the causal agent of fire blight. Moreover, these two species share phenotypic and molecular characteristics. Two specific and sensitive conventional and real-time PCR protocols were developed to identify and detect E. piriflorinigrans and to differentiate it from E. amylovora and other species of this genus. These protocols were based on sequences from plasmid pEPIR37, which is present in all strains of E. piriflorinigrans analyzed. After the stability of the plasmid was demonstrated, the specificities of the protocols were confirmed by the amplification of all E. piriflorinigrans strains tested, whereas 304 closely related pathogenic and nonpathogenic Erwinia strains and microbiota from pear trees were not amplified. In sensitivity assays, 10 3 cells/ml extract were detected in spiked plant material by conventional or real-time PCR, and 10 2 cells/ml were detected in DNA extracted from spiked plant material by real-time PCR. The protocols developed here succeeded in detecting E. piriflorinigrans in 102 out of 564 symptomatic and asymptomatic naturally infected pear samples (flowers, cortex stem tissue, leaves, shoots, and fruitlets), in necrotic Pyracantha sp. blossoms, and in necrotic pear and apple tissues infected with both E. amylovora and E. piriflorinigrans. Therefore, these new tools can be used in epidemiological studies that will enhance our understanding of the life cycle of E. piriflorinigrans in different hosts and plant tissues and its interaction with E. amylovora. Erwinia piriflorinigrans is a Gram-negative plant-pathogenic bacterium causing pear blossom necrosis (1). The disease affects pear production and can reduce fruit yield. It was first observed in Valencia, Spain, in 1999 (2, 3). After the first identification, the disease was observed at the same place in later years (1). Due to its recent discovery, the biology, ecology, and life cycle of this new species are still poorly understood.Unlike Erwinia amylovora, the causal agent of fire blight, E. piriflorinigrans affects blossoms and not other parts of plants (3). Nevertheless, E. piriflorinigrans colonies can be easily mistaken for E. amylovora in culture media, e.g., CCT medium (4), King's medium B (5), and sucrose nutrient agar (SNA) or Levan medium, which are usually utilized and recommended for the isolation of E. amylovora (6, 7). These two pathogens show similar metabolic profiles by use of the commercial API 20E, API 20NE, API ZYM, and API 50CH strips (bioMérieux, France), as well as close fatty acid profiles. E. piriflorinigrans can react with several antisera, and even with one of the monoclonal antibodies, used to detect E. amylovora (3). Moreover, E. piriflorinigrans reacts positively in PCR using the 23S rRNA gene sequence-based primers de...

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Nucleotide Sequences, Genetic Organization, and Distribution of pEU30 and pEL60 from Erwinia amylovora

Cited by 52 publications

References 22 publications

Genomics and current genetic understanding of Erwinia amylovora and the fire blight antagonist Pantoea vagans

Genomics and current genetic understanding of Erwinia amylovora and the fire blight antagonist Pantoea vagans

F-Like Type IV Secretion Systems Encode Proteins with Thioredoxin Folds That Are Putative DsbC Homologues

Conventional and Real-Time PCRs for Detection of Erwinia piriflorinigrans Allow Its Distinction from the Fire Blight Pathogen, Erwinia amylovora

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