Discrimination of <Emphasis Type="Italic">Pseudomonas syringae</Emphasis> isolates from sweet and wild cherry using rep-PCR

Bacterial canker is one of the most important diseases of cherry (Prunus avium). This disease can be caused by two pathovars of Pseudomonas syringae: pv. morsprunorum and pv. syringae. Repetitive DNA polymerase chain reaction-based fingerprinting (rep-PCR) was investigated as a method to distinguish pathovars, races and isolates of P. syringae from sweet and wild cherry. After amplification of total genomic DNA from 87 isolates using the REP (repetitive extragenic palindromic), ERIC (enterobacterial repetitive intergenic consensus) and BOX primers, followed by agarose gel electrophoresis, groups of isolates showed specific patterns of PCR products. Pseudomonas syringae pv. syringae isolates were highly variable. The differences amongst the fingerprints of P. syringae pv. morsprunorum race 1 isolates were small. The patterns of P. syringae pv. morsprunorum race 2 isolates were also very uniform, with one exception, and distinct from the race 1 isolates. rep-PCR is a rapid and simple method to identify isolates of the two races of P. syringae pv. morsprunorum; this method can also assist in the identification of P. syringae pv. syringae isolates, although it cannot replace inoculation on susceptible hosts such as cherry and lilac.     

Identification of pathovars and races of <Emphasis Type="Italic">Pseudomonas syringae,</Emphasis> the main causal agent of bacterial disease in pea in North-Central Spain,and the search for disease resistance

A total of 298 bacterial isolates were collected from pea cultivars, landraces and breeding lines in North-Central Spain over several years. On the basis of biochemical-physiological characteristics and molecular markers, 225 of the isolates were identified as Pseudomonas syringae, either pv. pisi (110 isolates) or pv. syringae (112), indicating that pv. syringae is as frequent as pv. pisi as causal agent of bacterial diseases in pea. Most strains (222) were pathogenic on pea. Further race analyses of P. syringae pv. pisi strains identified race 4 (59.1% of the isolates of this pathovar), race 2 (20.0%), race 6 (11.8%), race 5 (3.6%) and race 3 (0.9%). Five isolates (4.6%) showed a not-previously described response pattern on tester pea genotypes, which suggests that an additional race 8 could be present in P. syringae pv. pisi. All the isolates of P. syringae pv. syringae were highly pathogenic when inoculated in the tester pea genotypes, and no significant pathogenic differences were observed. Simultaneous infections with P. syringae pv. pisi and pv. syringae in the same fields were observed, suggesting the importance of resistance to both pathovars in future commercial cultivars. The search for resistance among pea genotypes suitable for production in this part of Spain or as breeding material identified the presence of resistance genes for all P. syringae pv. pisi races except for race 6. The pea cultivars Kelvendon Wonder, Cherokee, Isard, Iceberg, Messire and Attika were found suitable sources of resistance to P. syringae pv. syringae.     

Multiphasic Approach for the Identification of the Different Classification Levels Of Pseudomonas savastanoi Pv. Phaseolicola

The relationships between strains of Pseudomonas savastanoi pv. phaseolicola (P. sav. phaseolicola), P. syringae pv. tabaci (P. syr. tabaci) and P. syr. syringae which all cause disease on bean; the related species P. sav. glycinea and P. syr. actinidiae, and reference bacteria, were evaluated by studying the phenotypic and genetic diversity of a collection of 62 strains. All the P. sav. phaseolicola strains tested produced characteristic watersoaked lesions on bean pods. Other pathovars produced varying combinations of symptoms including necrotic lesions, with or without watersoaked centres and sunken tissue collapse of the lesion (P. syr. tabaci) and necrotic lesions with or without sunken collapse (P. syr. syringae). At the genomospecies level, all the strains of P. sav. phaseolicola, P. sav. glycinea and P. syr. tabaci, belonging to genomospecies 2, could be separated from P. syr. syringae strains (genomospecies 1) and P. syr. actinidiae strains (unknown genomospecies) by BOX-PCR and DNA/DNA hybridisation. To distinguish P. sav. phaseolicola, within genomospecies 2, from P. sav. glycinea and P. syr. tabaci, it was necessary to perform nutritional characterisations myo-inositol negative and p-hydroxy benzoate positive for P. sav. phaseolicola strains), PCR with specific primers designed from the tox region (positive for all of the P. sav. phaseolicola strains) and serotyping, as 71% of the P. sav. phaseolicola strains reacted as O-serogroup PHA1. Important intrapathovar variation was seen by genomic fingerprinting with REP and ERIC primers, as well as with RAPD primers (AE7 and AE10) and esterase profilings. While RAPD fingerprinting detected variability correlated with two race-associated evolutionary lines, REP, ERIC and esterase profiles revealed intrapathovar variation linked to some host origins, that separated the kudzu isolates, and the mungbean isolates, from the other P. sav. phaseolicola strains.     

A strain ofPseudomonas syringae which does not belong to pathovarphaseolicola produces phaseolotoxin

A bacterial strain, CFBP 3388, isolated from Vetch (Vicia sativa, L.) was identified asP. s. pv.syringae on the basis of nutritional and biochemical patterns which were obtained with classical tests and the Biolog system. It caused necrotic symptoms typical ofP. s. pv.syringae on bean leaves and pods after artificial inoculation. However, the isolate caused a citrulline-reversible inhibition ofE. coli in phaseolotoxin bioassay. Furthermore, with CFBP 3388 DNA as template a 1900 bp DNA fragment, specific for the phaseolotoxin DNA cluster ofP. s. pv.phaseolicola, was amplified by PCR. This is the first demonstration that an isolate ofP. syringae that is not pv.phaseolicola can produce phaseolotoxinAbbreviations bp base pair - kb kilobase - OCT Ornithine Carbamoyl Transferase     

Resistance to Pseudomonas syringae in a collection of pea germplasm under field and controlled conditions

A total of 242 Pisum accessions were screened for resistance to Pseudomonas syringae pv. pisi under controlled conditions. Resistance was found to all races, including race 6 and the recently described race 8. Fifty‐eight accessions were further tested for resistance to P. syringae pv. syringae under controlled conditions, with some highly resistant accessions identified. Finally, a set of 41 accessions were evaluated for resistance to P. syringae pv. pisi and pv. syringae under spring‐ and winter‐sowing field conditions. R2, R3 and R4 race‐specific resistance genes to P. syringae pv. pisi protected pea plants in the field. Resistance sources to race 6 identified under controlled conditions were ineffective in the field. Frost effects were also evaluated in relation to disease response. Results strongly suggest that frost tolerance is effective in lowering the disease effects caused by P. syringae pv. pisi and pv. syringae under frost‐stress conditions, even in the absence of disease resistance genes, although the highest degree of this protection is reached when frost tolerance and disease‐resistance genes are combined in the same genetic background.     

The Use of Bioluminescence for Monitoring in planta Growth Dynamics of a Pseudomonas syringae Plant Pathogen

The use of bioluminescence was evaluated as a tool to study Pseudomonas syringae population dynamics in susceptible and resistant plant environments. Plasmid pGLITE, containing the luxCDABE genes from Photorhabdus luminescens, was introduced into Pseudomonas syringae pv. phaseolicola race 7 strain 1449B, a Gram-negative pathogen of bean (Phaseolus vulgaris). Bacteria recovered from plant tissue over a five-day period were enumerated by counting numbers of colony forming units and by measurement of bioluminescence. Direct measurement of bioluminescence from leaf disc homogenates consistently reflected bacterial growth as determined by viable counting, but also detected subtle effects of the plant resistance response on bacterial viability. This bioluminescence procedure enables real time measurement of bacterial metabolism and population dynamics in planta, obviates the need to carry out labour intensive and time consuming traditional enumeration techniques and provides a sensitive assay for studying plant effects on bacterial cells.     

Cellular reactions in Arabidopsis following challenge by strains of Pseudomonas syringae: From basal resistance to compatibility

Reactions to strains of the bean halo-blight pathogen Pseudomonas syringae pv. phaseolicola (Pph) strain 1448A and the Arabidopsis and tomato pathogen P.s. pv. tomato (Pst) strain DC3000 were examined by transmission electron microscopy. Wild-type and hrpL mutant strains of Pph failed to multiply in the accession Columbia (Col)-5, but did not cause a hypersensitive reaction (HR). Symptomless non-host resistance to 1448A and the hrpL mutant was associated with the progressive alteration of the plant cell wall adjacent to bacteria, following the accumulation of membrane bound vesicles within the cytoplasm at reaction sites. Large papillae containing callose accumulated within challenged plant cells. Papillae also formed in the pmr4–1 mutant of Col-0 which lacks an inducible callose synthase but immunocytochemical labelling demonstrated that they contained very little β-1, 3 glucan. Some papillae formed in Col-5 in response to the virulent pathogen DC3000, but they dispersed during cell collapse and lesion formation. Transconjugants of Pph expressing the avirulence genes avrPpiA and avrPphB matching the RPM1 and RPS5 resistance genes, caused rapid and slow HR development, respectively. Although corpse morphology was observed our observations suggest that in Arabidopsis, plant cell death during the HR is programmed but represents a variant of necrosis rather than apoptosis. Cerium chloride staining revealed the accumulation of H₂O₂ at reaction sites. The strongest H₂O₂ response was found during the HR activated by avrPpiA but localised generation of peroxide was also found at sites of papilla deposition next to 1448A or the hrpL mutant. Accumulation of H₂O₂ during the HR, but not during wall alterations, was strongly suppressed by inhibition of NADPH oxidase. The differential effect of the inhibitor suggests an alternative source of H₂O₂ to modify the plant wall. Extension of peroxide-driven cross-linking reactions to bacterial cell walls may contribute to the restriction of bacterial multiplication. The lowest level of H₂O₂ occurred during the compatible reaction to DC3000. Characterisation of the cellular co-ordination of basal (non-host) resistance has revealed several potential targets for bacterial effector proteins.     

Genetic analyses of Pseudomonas syringae isolates from Belgian fruit orchards reveal genetic variability and isolate-host relationships within the pathovar syringae, and help identify both races of the pathovar morsprunorum

A collection of Pseudomonas syringae and viridiflava isolates was established between 1993 and 2002 from diseased organs sampled from 36 pear, plum and cherry orchards in Belgium. Among the 356 isolates investigated in this study, phytotoxin, siderophore and classical microbiology tests, as well as the genetical methods REP-, ERIC- and BOX- (collectively, rep-) and IS50-PCR, enabled identification to be made of 280 isolates as P. syringae pv. syringae (Pss), 41 isolates as P. syringae pv. morsprunorum (Psm) race 1, 12 isolates as Psm race 2, three isolates as P. viridiflava and 20 isolates as unclassified P. syringae. The rep-PCR methods, particularly BOX-PCR, proved to be useful for identifying the Psm race 1 and Psm race 2 isolates. The latter race was frequent on sour cherry in Belgium. Combined genetic results confirmed homogeneities in the pvs avii, and morsprunorum race 1 and race 2 and high diversity in the pv. syringae. In the pv. syringae, homogeneous genetic groups consistently found on the same hosts (pear, cherry or plum) were observed. Pathogenicity on lilac was sometimes variable among Pss isolates from the same genetic group; also, some Psm race 2 and unclassified P. syringae isolates were pathogenic to lilac. In the BOX analyses, four patterns included 100% of the toxic lipodepsipeptide (TLP)-producing Pss isolates pathogenic to lilac. Many TLP-producing Pss isolates non-pathogenic to lilac and the TLP-non-producing Pss isolates were classified differently. Pseudomonas syringae isolates that differed from known fruit pathogens were observed in pear, sour cherry and plum orchards in Belgium.     

Defense responses of Arabidopsis thaliana inoculated with Pseudomonas syringae pv. tabaci wild type and defective mutants for flagellin (ΔfliC) and flagellin-glycosylation (Δorf1)

Flagellin, an essential component of the bacterial flagellar filament, is capable of inducing a hypersensitive response (HR), including cell death, in a nonhost plant. A flagellin-defective mutant (ΔfliC) of Pseudomonas syringae pv. tabaci lacks both the flagellar filament and motility, whereas a flagellin-glycosylation-defective mutant (Δorf1) retains the flagellar filament but lacks the glycosyl modification of flagellin protein. To investigate the role of flagellin protein and its glycosylation in the interaction with its nonhost Arabidopsis thaliana, we analyzed plant responses after inoculation with these bacteria. Inoculation with wild-type P. syringae pv. tabaci induced HR, with the generation of reactive oxygen species and cell death. In contrast, inoculation with either ΔfliC or Δorf1 mutant induced a low level of HR, and inoculated leaves developed a disease-like yellowing. These mutant bacteria multiplied better than the wild-type bacteria in A. thaliana. These results indicate that A. thaliana expresses a defense reaction in response to the bacterial flagellin with its glycosyl structure.     

The use of PCR melting profile for typing of <Emphasis Type="Italic">Pseudomonas syringae</Emphasis> isolates from stone fruit trees

Of thirty fluorescent Pseudomonas isolates originating from symptomatic tissues of sweet (Prunus avium) and sour cherry (Prunus cerasus), plum (Prunus domestica), peach (Prunus persica) and apricot (Prunus armeniaca), 23 were identified as P. syringae using LOPAT tests. Further characterization of those isolates by GATTa and L-lactate utilization tests showed that 10 of them belonged to race 1, six to race 2 of P. syringae pv. morsprunorum (Psm) and six other isolates were identified as pathovar syringae (Pss). One isolate (791) was determined as atypical. Phenotypic determination and genetic analysis of studied isolates for toxin production revealed that isolates of Pss produced syringomycin, 3 Psm race 1 produced coronatine and 6 Psm race 2 produced yersiniabactin. Genetic diversity of all isolates was evaluated with the PCR melting profile (PCR MP) method. A dendrogram constructed with PCR MP patterns showed positive correlation with phenotypically distinguished pathovars. Isolates of Psm races 1 and 2 formed distinct, tight clusters, whereas Pss isolates were more heterogeneous. Isolate 791 was placed within Pss isolates. Bacteria identified as Pss caused more severe symptoms on immature cherry fruits compared to Psm, which corresponded to determined pathovars and races.     

Characterization of the pathogenicity of strains of Pseudomonas syringae towards cherry and plum

Bacterial canker is a major disease of Prunus avium (cherry), Prunus domestica (plum) and other stone fruits. It is caused by pathovars within the Pseudomonas syringae species complex including P. syringae pv. morsprunorum (Psm) race 1 (R1), Psm race 2 (R2) and P. syringae pv. syringae (Pss). Psm R1 and Psm R2 were originally designated as the same pathovar; however, phylogenetic analysis revealed them to be distantly related, falling into phylogroups 3 and 1, respectively. This study characterized the pathogenicity of 18 newly genome‐sequenced P. syringae strains on cherry and plum, in the field and laboratory. The field experiment confirmed that the cherry cultivar Merton Glory exhibited a broad resistance to all clades. Psm R1 contained strains with differential specificity on cherry and plum. The ability of tractable laboratory‐based assays to reproduce assessments on whole trees was examined. Good correlations were achieved with assays using cut shoots or leaves, although only the cut shoot assay was able to reliably discriminate cultivar differences seen in the field. Measuring bacterial multiplication in detached leaves differentiated pathogens from nonpathogens and was therefore suitable for routine testing. In cherry leaves, symptom appearance discriminated Psm races from nonpathogens, which triggered a hypersensitive reaction. Pathogenic strains of Pss rapidly induced disease lesions in all tissues and exhibited a more necrotrophic lifestyle than hemibiotrophic Psm. This in‐depth study of pathogenic interactions, identification of host resistance and optimization of laboratory assays provides a framework for future genetic dissection of host–pathogen interactions in the canker disease.     

Plant amphipathic proteins delay the hypersensitive response caused by harpinPssandPseudomonas syringaepv.syringae

Harpin_Pssfrom the plant pathogenPseudomonas syringaepv.syringaeis a proteinaceous elicitor that induces a hypersensitive response (HR) in non-host plants. The plant products which recognize harpin_Pssin the triggering of the HR are not yet known. According to the elicitor-receptor model, we hypothesize that an exogenous cell membrane receptor infiltrated into the intercellular space will interfere with the interaction between harpin_Pssand the putative receptor. We demonstrate a plant amphipathic protein (AP1) which can postpone the HR induced by harpin_Pssas well asP. syringaepv.syringae.AP1 was extracted by solubilizing proteins from healthy leaves in the non-polar n-octanol buffer followed by a polar Tris buffer. The amphipathic extracts were then further separated by gel filtration and anion exchange chromatography to obtain highly purified AP1. Similar proteins can be extracted from cotton, tomato, and sweet pepper. The N-terminal amino acid sequence of AP1 is conserved among cotton, tomato, and sweet pepper. The postponement of the harpin_Pss-mediated HR was characterized as a competitive dosage-dependent pattern of AP1. An analysis of the bacterial population development indicates that the effect of AP1 on the postponement of bacteria-mediated HR was attributed to the suppression of bacterial growth during the early stages of the HR. The time course analysis of the infiltration indicates that the postponement of HR resulted from the co-interaction between AP1 and the bacteria. Based on these results, we suggest that the postponement of bacteria-mediated HR is due to the interference of the interaction between harpin_Pssand the putative receptor in the plant. Our research provides a new approach to elucidating the role that plants may play in the nonhost response caused by pathogens.     

Detection and identification of the crucifer pathogen, <Emphasis Type="Italic">Xanthomonas campestris</Emphasis> pv. <Emphasis Type="Italic">campestris</Emphasis>, by PCR amplification of the conserved Hrp/type III secretion system gene <Emphasis Type="Italic">hrcC</Emphasis>

The development of a rapid detection method for Xanthomonas campestris pv. campestris (Xcc) in crucifer seeds and plants is essential for high-throughput certification purposes. Here we describe a diagnostic protocol for the identification/detection of Xcc by PCR amplification of fragments from the pathogenicity-associated gene hrcC. Under stringent conditions of amplification, a PCR product of 519 bp from hrcC was obtained from a collection of 46 isolates of Xcc, with the exception of two isolates from radish. No amplicons were obtained from 39 pure cultures of the phytopathogenic bacteria Xanthomonas campestris pv. cerealicola, X. campestris pv. juglandis, X. campestris pv. pelargonii, X. campestris pv. vitians, X. arboricola pv. pruni, X. axonopodis pv. phaseoli, X. axonopodis pv. vesicatoria, X. vesicatoria, Pseudomonas syringae pv. phaseolicola, P. syringae pv. syringae, P. syringae pv. tomato, P. fluorescens, P. marginalis, Pectobacterium atrosepticum, P. carotovorum subsp. carotovorum. In addition, PCR reactions were negative for fifty unidentified environmental isolates purified from the surface of crucifers. The PCR fragment was obtained from four strains previously classified as X. campestris pv. aberrans, X. campestris pv. armorociae, X. campestris pv. barbarae and X. campestris pv. incanae using pathogenicity assays. Our PCR protocol specifically detected Xcc in inoculated leaves, seeds and naturally infected leaves of crucifers.     

Differentiation of some pathovars of Pseudomonas syringae with monoclonal antibodies1

Two stable hybridoma clones secreting antibodies specific for three pathovars of Pseudomonas syringae were obtained from a fusion of murine myeloma cells with spleen cells of BALB/c mouse immunized with P. syringae pv. savastanoi. Undiluted hybridoma culture medium reacted strongly in indirect ELISA tests with 20 strains of pv. savastanoi, 10 strains of pv. tomato, and 3 strains of pv. papulans. There were no reactions with 23 (of 24) strains of pv. glycinea, three strains each of pvs pisi and tabaci, two strains of pv. tagetis and one each of pvs lachrymans and aptata. Hybridomas also reacted positively with six of 16 strains of pv. syringae and with one of three strains of pv. phaseolicola.     

Temperature, the GacS/GacA system, and host metabolites regulate the type VI secretion system of Pseudomonas syringae pv. phaseolicola

The recently discovered type VI secretion system (T6SS) is implicated in the pathogenic and/or virulence processes of diverse bacteria. The expression pattern of the T6SS differs among different organisms and also depends on several environmental factors. We initiated a study of the conditions that influence T6SS gene expression in Pseudomonas syringae pv. phaseolicola NPS3121. Our results indicate that low temperatures and plant extracts impact the expression of T6SS genes and that the process is subject to regulation by the GacS/GacA two-component system.     

Identification of two serological flagellar types (H1 and H2) inPseudomonas syringae pathovars

Flagellar antigen specificity was studied for the speciesPseudomonas syringae, P. viridiflava andP. cichorii. After checking their motility, bacteria were reacted against six polyclonal antisera containing anti-O (LPS) and anti-H (flagellar) antibodies by indirect immunofluorescent staining. Two distinct flagellar serotypes (H1 and H2) were described. The distribution of H1 and H2 serotypes was then determined for a collection of 88 phytopathogenicPseudomonas strains. Serotype H1 was possessed byP. syringae pv.aptata (12 strains),P. s. pv.helianthi (2),P. s. pv.pisi (11), andP. s. pv.syringae (13). Serotype H2 was possessed byP. cichorii (2),P. s. pv.delphinii (1),P. s. pv.glycinea (4),P. s. pv.lacrymans (1),P. s. pv.mori (1),P. s. pv.morsprunorum (10),P. s. pv.persicae (1),P. s. pv.phaseolicola (8),P. s. pv.tabaci (10) andP. s. pv.tomato (1).P. viridiflava (5) revealed HI, H2 and untyped flagella. The following isolates were untypable by the H1/H2 system:P. corrugata (3),P. fluorescens (2),P. tolaasii (1). H1/H2 serotypes distribution is not linked toP. syringae O-serogroups. On the other hand, H1/H2 distribution seems remarkably linked to the new genospecies of theP. syringae group.Abbreviations CFBP French Collection of Phytopathogenic Bacteria, Angers, France - ICMP International Collection of Micro-organisms from Plants, Auckland, New-Zealand - NCPPB National Collection of Plant Pathogenic Bacteria, Harpenden, Great Britain     

Harpinpsta from Pseudomonas syringae pv. tabaci Is Defective and Deficient in Its Expression and HR-inducing Activity

To elucidate the role of harpins produced by Pseudomonas syringae, the corresponding hrpZ gene was isolated from P. s. pv. tabaci. The sequence information revealed that this gene carries a serious mutation with 326 bp lacking in the central region and potentially encodes only 140 N-terminal amino acids because of a frame shift. The investigation of biological properties using recombinant harpin indicated harpin_psta was incapable of inducing HR in both host and nonhost plants. Based on an immunoblot analysis to detect harpin from P. s. pathovars in hrp-inducing medium, the truncated harpin_psta was neither expressed nor secreted into the culture medium. These results suggest that harpin is not the sole determinant of the host-parasite specificity in P. s. pv. tabaci. Received 10 August 2000/ Accepted in revised form 21 December 2000     

Pseudomonas syringae pv. avii (pv. nov.), the Causal Agent of Bacterial Canker of Wild Cherries (Prunus avium) in France

Bacterial strains isolated from cankers of wild cherry trees (Prunus avium) in France were characterized using numerical taxonomy of biochemical tests, DNA–DNA hybridization, repeat sequence primed-PCR (rep-PCR) based on REP, ERIC and BOX sequences, heteroduplex mobility assay (HMA) of internal transcribed spacer (ITS) as well as pathogenicity on wild cherry trees and other species of Prunus. They were compared to reference strains of Pseudomonas syringae pathovars isolated from wild and sweet cherry and various host plants. Wild cherry strains were closely related to P. syringae (sensu lato) in LOPAT group Ia (+ - - - +). Wild cherry strains were pathogenic to wild cherry trees and produced symptoms similar to those observed in orchards. They were pathogenic also, but at a lesser extent, to sweet cherry trees (cv. Napoléon). The wild cherry strains were collected from five different areas in France and appeared to constitute a very homogeneous group. They showed an homogenous profile of a biochemical and physiological characteristics. They were closely related by DNA–DNA hybridization and belonged to genomospecies 3 `tomato'. Rep-PCR showed that wild cherry strains constitute a tight group distinct from P. s. pv. morsprunorum races 1 and 2 and from other P. syringae pathovars. HMA profiles indicated that the ITS of all wild cherry strains were identical but different from P. s. pv. persicae strains since the two heteroduplex bands with reduced mobility were generated by hybridization with the P. s. pv. persicae pathotype strain CFBP 1573. The 8 genomospecies of Gardan et al. (1999) have not been converted into formal species as they cannot be differentiated by biochemical tests. Therefore, the pathovar system within P. syringae was currently used. P. syringae pv. avii is proposed for this bacterium causing a wild cherry bacterial canker and strain CFBP 3846 (NCPPB 4290, ICMP 14479) is designated as the pathotype.     

Oxidative stress regulates the expression of the Pht cluster genes involved in phaseolotoxin synthesis in <Emphasis Type="Italic">Pseudomonas syringae</Emphasis> pv. <Emphasis Type="Italic">phaseolicola</Emphasis> NPS3121

This study evaluated the role of oxidative stress on the expression of Pht cluster genes involved in phaseolotoxin synthesis in Pseudomonas syringae pv. phaseolicola. Results demonstrate that the expression of Pht cluster genes is regulated by oxidative stress in a manner dependent of the ROS present in the cell. The presence of H₂O₂ and Paraquat, influences on the expression of the Pht cluster genes in function of the compound and of the concentration evaluated, demonstrating that expression of Pht genes is part of the oxidative stress response in P. syringae pv. phaseolicola NPS3121.