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PubMedDate not supplied

Avirulence gene avrPphC from Pseudomonas syringae pv. phaseolicola 3121: a plasmid-borne homologue of avrC closely linked to an avrD allele.

Cosmid clone pPsp01 from race 1 Pseudomonas syringae pv. phaseolicola isolate 3121 conferred a unique pattern of soybean cultivar reactions when expressed in P. s. pv. glycinea R4. The avirulence phenotype was shown to result from the presence in clone pPsp01 of an avrD allele as well as an additional avirulence gene located approximately 5-kb upstream. The new gene, called avrPphC, shows high identity to and is phenotypically identical to avrC, previously cloned from P. s. pv. glycinea race 0. avrD and avrPphC occur on an approximately 120-kb indigenous plasmid in P. s. pv. phaseolicola 3121. Although commonly observed in Xanthomonas campestris, this is the first noted occurrence of multiple avirulence genes on a single plasmid in Pseudomonas syringae. Unlike avrD, however, avrPphC does not appear to occur widely in pathovars of Pseudomonas syringae.

Amino Acid Sequence↗
PubMedDate not supplied

Characterization of avrPphE, a gene for cultivar-specific avirulence from Pseudomonas syringae pv. phaseolicola which is physically linked to hrpY, a new hrp gene identified in the halo-blight bacterium.

The avirulence gene matching the R2 gene for resistance to halo-blight disease in Phaseolus was cloned and sequenced from race 4 strain 1302A of Pseudomonas syringae pv. phaseolicola. The predicted 41-kDa AvrPphE protein is hydrophilic, has no features that indicate function, and no similarity to other protein sequences. The promoter region of avrPphE contains a "harp box" motif. The gene was expressed more strongly in minimal than in nutrient-rich media. Lower concentrations of the phytoalexin phaseollin accumulated in tissue undergoing the hypersensitive reaction (HR) determined by avrPphE than by avrPphB. Homologs of avrPphE were detected in strains representing eight races of P. s. pv. phaseolicola including those virulent on cultivars with the R2 resistance gene, and in P. s. pv. tabaci but not in P. cichorii or P. s. pvs. coronafaciens, glycinea, maculicola, pisi, or syringae. Disruption of avrPphE prevented induction of the HR but did not appear to affect basic pathogenicity. Transposon mutagenesis and DNA sequencing showed that avrPphE was linked to hrpY a hrp locus identified at the left end of the hrp gene cluster. Sequence analysis showed that the region linked to avrPphE was very similar to DNA containing hrp genes from P. s. pv. syringae including hrpJ, hrpL, and hrpK.

Amino Acid Sequence↗
PubMedDate not supplied

Characterization of avrE from Pseudomonas syringae pv. tomato: a hrp-linked avirulence locus consisting of at least two transcriptional units.

Cosmid clone pPT10E9 from Pseudomonas syringae pv. tomato caused P. s pv. glycinea to elicit the HR on leaves of all tested soybean cultivars. The avirulence function of pPT10E9, called avrE, occurred on an 11.3-kb DNA fragment located immediately adjacent to the P. s. pv. tomato hrp gene cluster. Tn3-gus saturation mutagenesis of the avrE locus and adjacent DNA revealed at least four transcriptional units occurring immediately adjacent to the hrpRS locus that were all regulated in a manner similar to hrp genes (induced only in minimal induction media or in planta and required the hrpL and hrpRS loci for expression). Transcriptional units III and IV, but not II or V, were required for avrE function. P. s. pv. tomato DC3000 carrying mutations in each of the four transcripts retained full virulence on tomato leaves and elicited the HR on tobacco and soybean plants. This was unlike strain PT23, where mutation of avrE greatly decreased virulence on tomato leaves. The promoter regions for three of the investigated transcriptional units contained a consensus sequence occurring in the promoter regions of several other P. syringae avirulence and hrp genes. The promoter region of transcriptional unit IV, required for avrE function, did not contain such a sequence, but included an element which may function as a sigma-54 promoter. Introduction of the cloned P. s. pv. tomato avrE locus into five other P. syringae pathovars did not cause them to elicit the HR on their normal host plants.

Bacterial Proteins↗
PubMedDate not supplied

The avrRpm1 gene of Pseudomonas syringae pv. maculicola is required for virulence on Arabidopsis.

We demonstrate that the avirulence gene avrRpm1, isolated from Pseudomonas syringae pv. maculicola strain Psm M2 via interaction with the Arabidopsis resistance gene RPM1, is also required for maximal virulence on this host. Two avrRpm1::Tn3-Spice marker-exchange mutants do not elicit a hypersensitive reaction on RPM1-containing Arabidopsis accessions Col-0 and Oy-0. Surprisingly, these mutants neither generate disease symptoms, nor grow in planta, after inoculation onto susceptible accessions Nd-0, Fe-1, and Mt-0. These deficiencies can be corrected in a merodiploid containing a wild-type avrRpm1 allele, and are not observed following gene-replacement with avrRpm1::Tn3-Spice alleles containing insertions just beyond the 3' terminus of the avirulence gene open reading frame. AvrRpm1 mRNA is expressed in low, but detectable amounts, in rich media. Induced accumulation of transcript is observed 3 h after shift to minimal media, and an avrRpm1::Tn3-Spice marker-exchanged reporter gene reaches maximal induction 30 min after shift. AvrRpm1 transcription starts 5 base-pairs 3' of the putative regulatory "hrp-box" cis-element found upstream of many P. syringae avr and hrp genes. Transcriptional induction of the marker-exchanged reporter gene in minimal media is enhanced by a carbon source. Induction in planta is the same in either resistant or susceptible Arabidopsis accessions, and is unaffected by the presence or absence of wild-type avrRpm1. As previously observed for many other P. syringae avr genes, transcriptional regulation of avrRpm1 in minimal media is dependent on hrpL and hrpS.

Arabidopsis↗
PubMed2001

Functional analysis of the type III effectors AvrRpt2 and AvrRpm1 of Pseudomonas syringae with the use of a single-copy genomic integration system.

Gram-negative phytopathogenic bacteria require a type III secretion apparatus for pathogenesis, presumably to deliver Avr effector proteins directly into plant cells. To extend previous studies of Avr effectors that employed plasmids encoding Avr proteins, we developed a system that permits the integration of any gene into the Pseudomonas syringae genome in single copy. With this system, we confirmed earlier findings showing that P. syringae pv. maculicola strain PsmES4326 expressing the AvrRpt2 effector induces a resistance response in plants with the cognate R gene, RPS2. Chromosomally located avrRpt2, however, provoked a stronger resistance response than that observed with plasmid-expressed AvrRpt2 in RPS2+ plants. Additionally, chromosomal expression of AvrRpt2 conferred a fitness advantage on P. syringae grown in rps2- plants, aiding in growth within leaves and escape to leaf surfaces that was difficult to detect with plasmid-borne avrRpt2. Finally, with the use of the genomic integration system, we found that a chimeric protein composed of the N terminus of the heterologous AvrRpml effector and the C-terminal effector region of AvrRpt2 was delivered to plant cells. Because the C terminus of AvrRpt2 cannot translocate into plant cells on its own, this indicates that the N-terminal region can direct secretion and translocation during an infection, which supports the view that Avr proteins have a modular design. This work establishes a readily manipulatable system to study type III effectors in a biologically realistic context.

Arabidopsis↗
PubMed2001

Isolation and characterization of the gene coding for the amidinotransferase involved in the biosynthesis of phaseolotoxin in Pseudomonas syringae pv. phaseolicola.

Pseudomonas syringae pv. phaseolicola is the causal agent of the "halo blight" disease of beans. A key component in the development of the disease is a nonhost-specific toxin, Ndelta-(N'-sulphodiaminophosphinyl)-ornithyl-alanyl-homoarginine, known as phaseolotoxin. The homoarginine residue in this molecule has been suggested to be the product of L-arginine:lysine amidinotransferase activity, previously detected in extracts of P. syringae pv. phaseolicola grown under conditions of phaseolotoxin production. We report the isolation and characterization of an amidinotransferase gene (amtA) from P. syringae pv. phaseolicola coding for a polypeptide of 362 residues (41.36 kDa) and showing approximately 40% sequence similarity to L-arginine:inosamine-phosphate amidinotransferase from three species of Streptomyces spp. and 50.4% with an L-arginine:glycine amidinotransferase from human mitochondria. The cysteine, histidine, and aspartic acid residues involved in substrate binding are conserved. Furthermore, expression of the amtA and argK genes and phaseolotoxin production occurs at 18 degrees C but not at 28 degrees C. An amidinotransferase insertion mutant was obtained that lost the capacity to synthesize homoarginine and phaseolotoxin. These results show that the amtA gene isolated is responsible for the amidinotransferase activity detected previously and that phaseolotoxin production depends upon the activity of this gene.

Amidinotransferases↗
PubMed1999

A dispensable region of the chromosome which is associated with an avirulence gene in Pseudomonas syringae pv. pisi.

Pseudomonas syringae pv. pisi comprises a number of races which fall into two phylogenetically distinct groups (designated I and II). Races are based on cultivar specificity in the host plant, pea (Pisum sativum), and are specified by the presence of avirulence genes. The avirulence gene avrPpiA1 is present on the chromosome of all strains examined in race 2, which belongs to phylogenetic group II. A race 4B strain, from phylogenetic group I, lacks this avirulence gene and a comparative study was made of the chromosome in strains representing these two races. A race 2 cosmid clone (pAV270) carrying avrPpiA1 was used as a basis for collinearity analysis of races 2 and 4B. A region of the chromosome amounting to 8.5 kb and including avrPpiA1 was absent from race 4B compared with race 2. A fragment spanning the junction of the discontinuity in race 4B was isolated, cloned and used to delimit the extent of the additional DNA present in race 2. In both races the borders of the discontinuity contained DNA sequences which showed a high degree of conservation. A 7 bp slightly imperfect direct repeat (CCAGC(T)/(A)T) flanked the additional DNA in race 2, with a single copy in race 4B. The region flanking the additional DNA was present in all races of P. syringae pv. pisi. These results confirm the phylogenetic groupings in P. syringae pv. pisi.

Base Sequence↗
PubMed1999

Replication regions from plant-pathogenic Pseudomonas syringae plasmids are similar to ColE2-related replicons.

Many strains of the phytopathogen Pseudomonas syringae contain mutually compatible plasmids that share extensive regions of sequence homology and essential replication determinants. The replication regions of two compatible large plasmids involved in virulence or pathogenicity, pPT23A from P. syringae pv. tomato strain PT23 and pAV505 from P. syringae pv. phaseolicola strain HRI1302A, were isolated. DNA sequencing of the origins of replication revealed homologous ORFs, designated ORF-Pto and ORF-Pph, respectively. Both ORFs are 1311 bp long and encode peptides of 437 amino acids with predicted molecular masses of 48259 (Pto) and 48334 (Pph) Da. Expression of the two ORFs in Escherichia coli produced peptides of 50 kDa (Pto) and 56 kDa (Pph). The predicted peptides showed an overall identity of 897 %, being highly conserved from residues 1 to 373, but showing considerable variation in their C-terminal regions (50% identity over the last 64 aa). The two ORFs had significant similarity with the putative replication protein from plasmid pTiK12 of Thiobacillus intermedius and other CoIE2-related plasmids. However, both peptides were 100 residues longer than any of the known CoIE2-related rep sequences. Subcloning of fragments from the replication region of pPT23A revealed the presence of at least three incompatibility determinants, designated IncA, IncB and IncC. Partial sequencing of the region downstream of ORF-Pto revealed homology to the ru/AB genes, involved in UV resistance, from plasmid pPSR1. It is proposed that the replication origin of pPT23A serves as the prototype of a family of related plasmids.

Amino Acid Sequence↗
PubMed2002

Signals involved in Arabidopsis resistance to Trichoplusia ni caterpillars induced by virulent and avirulent strains of the phytopathogen Pseudomonas syringae.

Plants have evolved different but interconnected strategies to defend themselves against herbivorous insects and microbial pathogens. We used an Arabidopsis/Pseudomonas syringae pathosystem to investigate the impact of pathogen-induced defense responses on cabbage looper (Trichoplusia ni) larval feeding. Arabidopsis mutants [npr1, pad4, eds5, and sid2(eds16)] or transgenic plants (nahG) that are more susceptible to microbial pathogens and are compromised in salicylic acid (SA)-dependent defense responses exhibited reduced levels of feeding by T. ni compared with wild-type plants. Consistent with these results, Arabidopsis mutants that are more resistant to microbial pathogens and have elevated levels of SA (cpr1 and cpr6) exhibited enhanced levels of T. ni feeding. These experiments suggested an inverse relationship between an active SA defense pathway and insect feeding. In contrast to these results, there was increased resistance to T. ni in wild-type Arabidopsis ecotype Columbia plants that were infected with P. syringae pv. maculicola strain ES4326 (Psm ES4326) expressing the avirulence genes avrRpt2 or avrB, which elicit a hypersensitive response, high levels of SA accumulation, and systemic acquired resistance to bacterial infection. Similar results were obtained with other ecotypes, including Landsberg erecta, Cape Verdi Islands, and Shakdara. When infected with Psm ES4326(avrRpt2) or Psm ES4326(avrB), nahG transgenic and npr1 mutant plants (which are more susceptible to virulent and avirulent P. syringae strains) failed to show the increased insect resistance exhibited by wild-type plants. It was surprising that wild-type plants, as well as nahG and npr1 plants, infected with Psm ES4326 not expressing avrRpt2 or avrB, which elicits disease, became more susceptible to T. ni. Our results suggest two potentially novel systemic signaling pathways: a systemic response elicited by HR that leads to enhanced T. ni resistance and overrides the SA-mediated increase in T. ni susceptibility, and a SA-independent systemic response induced by virulent pathogens that leads to enhanced susceptibility to T. ni.

Animals↗
PubMed1991

Induction of Arabidopsis defense genes by virulent and avirulent Pseudomonas syringae strains and by a cloned avirulence gene.

We developed a model system to study the signal transduction pathways leading to the activation of Arabidopsis thaliana genes involved in the defense against pathogen attack. Here we describe the identification and characterization of virulent and avirulent Pseudomonas syringae strains that elicit disease or resistance symptoms when infiltrated into Arabidopsis leaves. The virulent and avirulent strains were characterized by determining growth of the pathogen in Arabidopsis leaves and by measuring accumulation of mRNA corresponding to Arabidopsis phenylalanine ammonia-lyase (PAL), beta-1,3-glucanase (BG), and chalcone synthase (CHS) genes in infected leaves. The virulent strain, P. syringae pv maculicola ES4326, multiplied 10(5)-fold in Arabidopsis leaves and strongly elicited BG1, BG2, and BG3 mRNA accumulation but had only a modest effect on PAL mRNA accumulation. In contrast, the avirulent strain, P. syringae pv tomato MM1065, multiplied less than 10-fold in leaves and had only a minimal effect on BG1, BG2, and BG3 mRNA accumulation, but it induced PAL mRNA accumulation. No accumulation of CHS mRNA was found with either ES4326 or MM1065. We also describe the cloning of a putative avirulence (avr) gene from the avirulent strain MM1065 that caused the virulent strain ES4326 to grow less well in leaves and to strongly elicit PAL but not BG1 and BG3 mRNA accumulation. These results suggest that the Arabidopsis PAL and BG genes may be activated by distinct signal transduction pathways and show that differences in plant gene induction by virulent and avirulent strains can be attributed to a cloned presumptive avr gene.

Cloning, Molecular↗
PubMed1996

Expression of the Pseudomonas syringae avirulence protein AvrB in plant cells alleviates its dependence on the hypersensitive response and pathogenicity (Hrp) secretion system in eliciting genotype-specific hypersensitive cell death.

The nonpathogenic bacteria Pseudomonas fluorescens and Escherichia coli can elicit a genotype-specific hypersensitive response (HR) in plants if they express both the HR and pathogenesis (Hrp) protein secretion system and the HrpZ harpin from P. syringae pv syringae 61 and a P. syringae avirulence (avr) gene whose presence is recognized by a corresponding disease resistance gene in the plant. We have found that the recognition event appears to require transfer of the Avr protein into the plant cell. Elicitation of a genotype-specific HR was observed with avrB+ P. fluorescens in soybean and Arabidopsis plants carrying resistance genes RPG1 and RPM1, respectively, and with avrPto+ E. coll in tomato plants carrying resistance gene PTO, but only if the Hrp secretion system, HrpZ, and the appropriate Avr proteins were produced in the same bacterial cell. The failure of avrB hyperexpression and exogenous AvrB or HrpZ to alleviate these requirements in soybean and Arabidopsis suggests that the site of AvrB action is not in the bacterial cell or plant apoplast. An Arabidopsis rps3 (rpm1) glabrous1 mutant was transformed with constructs expressing avrB and was crossed with an Arabidopsis ecotype Columbia (RPM1 GLABROUS1) plant. F1 seedlings (identified by their kanamycin-resistant, pubescent phenotype) exhibited extensive necrosis on cotyledon leaves 10 days postgermination. Ecotype Columbia and rps3-1 leaves biolistically cobombarded with plasmids expressing the beta-glucuronidase (GUS) gene and avrB failed to produce GUS activity (indicative of cell death) only when RPM1 and avrB were present in the leaf. Thus, both stable and transient expression of avrB in Arabidopsis resulted in RPM1-dependent necrosis, and the only demonstrable site of action for AvrB was inside plant cells.

Arabidopsis↗
PubMed1994

Evaluation of determinative tests for pathovars of Pseudomonas syringae van Hall 1902.

The utility of 36 presumptive determinative tests for 32 pathovars of Pseudomonas syringae was investigated. A total of 395 strains was examined. Most strains of 12 of these pathovars (Ps. syringae pv. cannabina, Ps. syr. delphinii, Ps. syr. glycinea, Ps. syr. helianthi, Ps. syr. lachrymans, Ps. syr. mori, Ps. syr. morsprunorum, Ps. syr. phaseolicola, Ps. syr. 'porri', Ps. syr. papulans, Ps. syr. savastanoi and Ps. syr. tabaci) formed clusters when test data were compared by centroid analysis. Pseudomonas syr. syringae, Ps. syr. aptata, Ps. syr. atrofaciens, Ps. syr. dysoxyli and Ps. syr. japonica formed a single cluster, indicating their possible synonymy. Strains of Ps. syr. antirrhini and Ps. syr. tomato were indistinguishable, as were those of Ps. syr. garcae and Ps. syr. oryzae. Strains of Ps. syr. berberidis, Ps. syr. coronafaciens, Ps. syr. eriobotryae, Ps. syr. maculicola, Ps. syr. passiflorae, Ps. syr. pisi and Ps. syr. striafaciens and Ps. syr. tagetis did not form distinguishable clusters. The tests which reliably differentiated pathovars are recorded in a determinative scheme.

Cluster Analysis↗
PubMed1993

The cloning and characterization of phage promoters, directing high expression of luciferase in Pseudomonas syringae pv. phaseolicola, allowing single cell and microcolony detection.

Regions of DNA containing promoter sequences from a Pseudomonas syringae pv. phaseolicola-specific phage (phi 11P) were identified by shotgun cloning into a broad-host-range promoter-probe vector (pQF70). When used in conjunction with the luciferase reporter genes, one of these DNA fragments, 19H, directed gene expression at a level which enabled the subsequent light output (bioluminescence) of single cells of P. syringae pv. phaseolicola to be detected and visualized using a charge-coupled device (CCD). The P. syringae pv. phaseolicola phi 11P, 19H and P. aeruginosa phi PLS27, HcM promoters gave a 50-fold increase in bioluminescence (maximum relative light output) compared to similar constructs containing other well-characterized promoters, for example, tetracycline. Similar bioluminescent characteristics of the transformed bacterium, were observed during growth with and without antibiotic-selection. When lux+ bacteria were inoculated onto French bean leaf (Phaseolus vulgaris L.), the resultant secondary halo blight lesions were bioluminescent and during phylloplane colonization by the lux+ bacterium, bioluminescence on leaf surfaces was detected and imaged by the CCD. Use of these newly identified promoters, combined with the greatly increased sensitivity of bioluminescence detection by the CCD, thus provided a new dimension for the study of natural ecological populations during the bacterial colonization of plants.

Cloning, Molecular↗
PubMed1995

The hrpRS locus of Pseudomonas syringae pv. phaseolicola constitutes a complex regulatory unit.

The right part of the hrp cluster of Pseudomonas syringae pv. phaseolicola contains two regulatory genes, the previously described hrpS gene and an adjacent locus, hrpR. In this study we determined the sequence of hrpR and analysed the functional organization of the two genes. HrpR and HrpS show high sequence similarities to each other and to other response regulators of the two-component regulatory system. This has recently also been described for the hrpRS system of the closely related pathogen Pseudomonas syringae pv. syringae. The results of our genetic analyses strongly indicate that hrpS expression is regulated by the hrpR gene product. DNA-protein binding studies and site-directed mutagenesis of the hrpR sequence provided further evidence that HrpR activates hrpS transcription by binding to an activator site. This HrpR binding site was mapped in a fragment which is located 378-609 nucleotides upstream of the hrpS transcription start site. The hrpS transcription start site maps 179 nucleotides upstream of the initiation codon ATG, as determined by primer extension analysis, and is preceded by a typical -12/-24 promoter motif.

Amino Acid Sequence↗
PubMed1996

Structure and activity of persicomycins, toxins produced by a Pseudomonas syringae pv. persicae/Prunus persica isolate.

A toxigenic property has been demonstrated in a Pseudomonas syringae pv. persicae/Prunus persica isolate. Several substances, which are named persicomycins, have been purified in variable quantities from cultures. The structures of four of them were established by NMR and chemical ionization mass spectrometry. These compounds are 3-(3'-hydroxy)hydroxy fatty acids and thus represent a new family among the phytobacterial toxins. Other minor substances have also been isolated and have been shown to belong to the same family on the basis of their 7H-NMR spectra. All of them cause necrosis of peach tree tissues, a symptom similar to the one obtained after bacterial infection and antibiosis of microorganisms such as Bacillus thuringiensis. These results provide evidence that necrosis-inducing toxins are not restricted to the pathovar syringae. Furthermore, similar substances were purified from necrosed tissues of inoculated and diseased peach trees. 3-(3'-Hydroxydecanoyloxy)hexadecenoic acid was isolated from both such tissues and from cultures, which strongly suggests a similar toxigenesis in vivo and in vitro. The involvement of persicomycins in the die-back disease of peach trees is now clearly established, which demonstrates that the toxigenic property of the bacterium participates in the disease. The phytotoxicity of the persicomycins is discussed in comparison with the lipodepsipeptide necrotic toxins of the syringae pathovar.

Anti-Bacterial Agents↗
PubMed2002

Construction of pMEKm12, an expression vector for protein production in Pseudomonas syringae.

Characterization of the biological roles of proteins is essential for functional genomics of pseudomonads. Heterologous proteins overproduced in Escherichia coli frequently fail to exhibit biological function. To circumvent this problem, vector pMEKm12 was constructed and used to overexpress proteins in Pseudomonas. The vector contains the pRO1600 replication origin, the maltose-binding protein (MBP) fusion system, and an inducible tac promoter. The pMEKm12 was successfully used to overexpress the syringomycin synthetase SyrB1 protein fused to MBP in Pseudomonas syringae pv. syringae. Furthermore, expression of the MBP-SyrB1 protein in the syrB1 mutant BR132A1 resulted in the restoration of syringomycin production. This vector will facilitate confirmation of the biochemical roles of nonribosomal peptide synthetase genes in Pseudomonas syringae, and studies of gene function from a wide spectrum of pseudomonads.

Bacterial Proteins↗
PubMed1983

Isolation and Partial Characterization of Bacteriophages of the Phytopathogen Pseudomonas syringae.

Bacteriophages isolated from culture supernatants of Pseudomonas syringae pv. syringae and from sewage were identified. The DNA from each phage was isolated and digested with the restriction endonuclease EcoRI. Eight isolates were determined to be different, with two phage isolates from sewage having restriction patterns identical to two phages from culture supernatants. The sizes of the phage DNA ranged from 24 to49 kilobases for isolates from sewage and from 39 to 52.5 kilobases for the isolates from culture supernatants. Buoyant densities of phage particles in CsCl varied from 1.498 to 1.507 g/cm for isolates from sewage and from 1.506 to 1.516 g/cm for isolates from culture supernatants. Electron microscopy revealed four morphological types. Based on plaque-forming ability of culture supernatants, 31 out of 47 strains of P. syringae are probably lysogenic.

Journal Article↗
PubMed1990

Plasmid-Determined Copper Resistance in Pseudomonas syringae from Impatiens.

A strain of Pseudomonas syringae was recently identified as the cause of a new foliar blight of impatiens. The bacterium was resistant to copper compounds, which are used on a variety of crops for bacterial and fungal disease control. The bacterium contained a single 47-kilobase plasmid (pPSI1) that showed homology to a copper resistance operon previously cloned and characterized from P. syringae pv. tomato plasmid pPT23D (D. Cooksey, Appl. Environ. Microbiol. 53:454-456, 1987). pPSI1 was transformed by electroporation into a copper-sensitive P. syringae strain, and the resulting transformants were copper resistant. A physical map of pPSI1 was constructed, and the extent of homology to pPT23D outside the copper resistance operon was determined in Southern hybridizations. The two plasmids shared approximately 20 kilobases of homologous DNA, with the remainder of each plasmid showing no detectable homology. The homologous regions hybridized strongly, but there was little or no conservation of restriction enzyme recognition sites.

Journal Article↗