Identification of a pathogenicity island, which contains genes for virulence and avirulence, on a large native plasmid in the bean pathogen<i>Pseudomonas syringae</i>pathovar phaseolicola

Jackson, Robert W.; Athanassopoulos, Evangelos; Tsiamis, George; Mansfıeld, John W.; Sesma, Ane; Arnold, Dawn L.; Gibbon, Marjorie J.; Murillo, Jesús; Taylor, John D.; Vivian, Alan

doi:10.1073/pnas.96.19.10875

Cited by 301 publications

(282 citation statements)

References 59 publications

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“…2) with high similarity to XerC, a prototypical phage integrase (tyrosine recombinase). Such genes have often been found near the beginning of chromosome regions thought to result from the horizontal transfer of DNA into the current host [7,8,10]. The gene next to the 818 integrase encodes a product of unknown function (ORF 2, Fig.…”

Section: I) Gene Transfer Blockmentioning

confidence: 99%

The Biosynthetic Gene Cluster for the β-Lactam Antibiotic Tabtoxin in Pseudomonas syringae

Kinscherf

Willis

2005

J Antibiot

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DNA sequence analysis revealed that the biosynthetic genes of the unusual b -lactam antibiotic tabtoxin reside at the att site adjacent to the lysC tRNA gene in Pseudomonas syringae BR2. ORFs encoded within the region included ones with similarity to b -lactam synthase and clavaminic acid synthase, as well as amino acid synthesis enzymes. Novel ORFs were present in a portion of the biosynthetic region associated with a toxin hypersensitivity phenotype. Tabtoxin resistance was associated with a fragment containing a major facilitator superfamily (MFS) transporter gene. (Fig. 1). The antibiotic is usually associated with bacteria of the Pseudomonas syringae species group causal to several types of chlorotic plant disease. While most b -lactam antibiotics exert their antimicrobial influence through the inhibition of bacterial cell wall synthesis, TBL appears to irreversibly inhibit the enzyme glutamine synthetase, causing cells to become intoxicated by high levels of their own unprocessed ammonia [3,4]. The genes encoding the pathway for both tabtoxin production and host resistance were originally cloned as a single cosmid insert from BR2, a Pseudomonas syringae strain causal to wildfire disease on bean [5]. Here we report the analysis of the DNA sequence of this cloned region.Subcloned fragments of the cosmid pRTBL823 were sequenced using a combination of primer walking with synthetic primers derived from endogenous sequence within the insert DNA and transposon priming (GPS-1, New England Biolabs). Sequence of plasmid miniprep DNA (Qiagen) was generated using dye terminator kits (ABI) analyzed by capillary electrophoresis (GeneAnalyser 310, ABI). The sequence of overlaps between subclones was confirmed by sequencing with the original cosmid

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Section: I) Gene Transfer Blockmentioning

confidence: 99%

The Biosynthetic Gene Cluster for the β-Lactam Antibiotic Tabtoxin in Pseudomonas syringae

Kinscherf

Willis

2005

J Antibiot

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“…Phospholipid-binding assays were carried out as described (29). To determine ␤-glucuronidase activity, plasmid pDGUS (30) carrying the E. coli uidA gene was introduced into Psph strains by triparental mating as described (27). GUS activity was quantified as described (30).…”

Section: Methodsmentioning

confidence: 99%

“…Pathogenicity tests of Psph strains on bean (Phaseolus vulgaris L.) were performed as described (27). Hemolytic activity was assayed as described (5).…”

Section: Methodsmentioning

confidence: 99%

HrpZPsph from the plant pathogen Pseudomonas syringae pv. phaseolicola binds to lipid bilayers and forms an ion-conducting pore invitro

Lee

Klüsener²,

Tsiamis³

et al. 2000

Proceedings of the National Academy of Sciences

120

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The hrp gene clusters of plant pathogenic bacteria control pathogenicity on their host plants and ability to elicit the hypersensitive reaction in resistant plants. Some hrp gene products constitute elements of the type III secretion system, by which effector proteins are exported and delivered into plant cells. Here, we show that the hrpZ gene product from the bean halo-blight pathogen, Pseudomonas syringae pv. phaseolicola (HrpZPsph), is secreted in an hrp-dependent manner in P. syringae pv. phaseolicola and exported by the type III secretion system in the mammalian pathogen Yersinia enterocolitica. HrpZPsph was found to associate stably with liposomes and synthetic bilayer membranes. Under symmetric ionic conditions, addition of 2 nM of purified recombinant HrpZ Psph to the cis compartment of planar lipid bilayers provoked an ion current with a large unitary conductivity of 207 pS. HrpZPsphrelated proteins from P. syringae pv. tomato or syringae triggered ion currents similar to those stimulated by HrpZPsph. The HrpZPsphmediated ion-conducting pore was permeable for cations but did not mediate fluxes of Cl ؊ . Such pore-forming activity may allow nutrient release and͞or delivery of virulence factors during bacterial colonization of host plants.

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“…3). Indeed, at least nine effectors have been described that enable a pathogen to suppress or evade HR-based PCD 21,26,27,[90][91][92][93][94] .…”

Section: Bacterial Suppression Of Hr-based Pcdmentioning

confidence: 99%

“…The effector protein VirPphA (also known as HopAB1) was the first example of an effector that modulated HR-based resistance 92 . It was observed that a normally virulent strain of P. syringae pv.…”

Section: Bacterial Suppression Of Hr-based Pcdmentioning

confidence: 99%

Bacterial elicitation and evasion of plant innate immunity

Abramovitch

Anderson

Martin

2006

Nat Rev Mol Cell Biol

373

285

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Recent research on plant responses to bacterial attack has identified extracellular and intracellular host receptors that recognize conserved pathogen-associated molecular patterns and more specialized virulence proteins, respectively. These findings have shed light on our understanding of the molecular mechanisms by which bacteria elicit host defences and how pathogens have evolved to evade or suppress these defences.Plants are a rich source of nutrients and water for microbes, and they are infected by many bacterial pathogens from both the Proteobacteria and Actinobacteria phyla (Supplementary information 1 (table)). Because of their broad host range, serious economic consequences and experimental tractability, the most intensively studied bacteria are members of the Proteobacteria phylum (such as Agrobacterium, Erwinia, Pseudomonas, Ralstonia and Xanthomonas) [1][2][3][4] . These pathogens are spread by wind, rain, insects or cultivation practices. They enter plant tissues either by wounds or through natural openings such as lenticels, hydathodes or stomata 5 , and they occupy the inter cellular spaces (apoplast) of various plant tissues or the xylem.Plant-pathogenic members of the Proteobacteria cause diverse disease symptoms, including specks, spots, blights, wilts, galls and cankers, and they can cause host-cell death in roots, leaves, flowers, fruits, stems and tubers (FIG. 1). These symptoms affect both yield and quality of agricultural crops and bacterial diseases can have serious economic, social and even political consequences [6][7][8] . Control of bacterial diseases is only partially effective and consists of copper-based sprays, antibiotics, biocontrol strategies, large-scale removal of infected plants and, most importantly, host genetic resistance 5 . Therefore, research on bacterial diseases of plants helps to elucidate fundamental aspects of microbial pathogenesis and associated host responses and also to develop more effective and sustainable disease-control methods.Correspondence to G.B.M. gbm7@cornell.edu. Competing interests statementThe authors declare no competing financial interests. DATABASES NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptPlant-pathogenic bacteria use virulence strategies that are either specialized to plant tissues or are broadly conserved among pathogens of both plants and animals (FIG. 1). Bacterial virulence is manifested as increases in the rate of growth or final population size, as well as by enhanced disease symptoms, which promote the spread of the pathogen through the plant or the broader environment.Unlike mammals, plants have a complex cell wall that bacteria must surmount to gain access to water and nutrients. Bacteria attack this barrier with extracellular virulence factors, such as cell wall degrading enzymes, and bypass it by the secretion of cell wall-permeable toxins 5 . However, perhaps the most effective virulence strategy, and one shared with animal bacterial pathogens, is to breach the wall by use of the type III s...

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Identification of a pathogenicity island, which contains genes for virulence and avirulence, on a large native plasmid in the bean pathogenPseudomonas syringaepathovar phaseolicola

Cited by 301 publications

References 59 publications

The Biosynthetic Gene Cluster for the β-Lactam Antibiotic Tabtoxin in Pseudomonas syringae

The Biosynthetic Gene Cluster for the β-Lactam Antibiotic Tabtoxin in Pseudomonas syringae

HrpZPsph from the plant pathogen Pseudomonas syringae pv. phaseolicola binds to lipid bilayers and forms an ion-conducting pore invitro

Bacterial elicitation and evasion of plant innate immunity

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