No data available that match "pseudomonas syringae"

Arabidopsis NHO1 is required for general resistance against Pseudomonas bacteria. (1/851)

Nonhost interactions are prevalent between plants and specialized phytopathogens. Although it has great potential for providing crop plants with durable resistance, nonhost resistance is poorly understood. Here, we show that nonhost resistance is controlled, at least in part, by general resistance. Arabidopsis plants are resistant to the nonhost pathogen Pseudomonas syringae pv phaseolicola NPS3121 and completely arrest bacterial multiplication in the plant. Ten Arabidopsis mutants were isolated that were compromised in nonhost (nho) resistance to P. s. phaseolicola. Among these, nho1 is caused by a single recessive mutation that defines a novel gene. nho1 is defective in nonspecific resistance to Pseudomonas bacteria, because it also supported the growth of P. s. tabaci and P. fluorescens bacteria, both of which are nonpathogenic on Arabidopsis. In addition, the nho1 mutation also compromised resistance mediated by RPS2, RPS4, RPS5, and RPM1. Interestingly, the nho1 mutation had no effect on the growth of the virulent bacteria P. s. maculicola ES4326 and P. s. tomato DC3000, but it partially restored the in planta growth of the DC3000 hrpS(-) mutant bacteria. Thus, the virulent bacteria appear to evade or suppress NHO1-mediated resistance by means of an Hrp-dependent virulence mechanism.  (+info)

Two pathways act in an additive rather than obligatorily synergistic fashion to induce systemic acquired resistance and PR gene expression. (2/851)

BACKGROUND: Local infection with necrotizing pathogens induces whole plant immunity to secondary challenge. Pathogenesis-related genes are induced in parallel with this systemic acquired resistance response and thought to be co-regulated. The hypothesis of co-regulation has been challenged by induction of Arabidopsis PR-1 but not systemic acquired resistance in npr1 mutant plants responding to Pseudomonas syringae carrying the avirulence gene avrRpt2. However, experiments with ndr1 mutant plants have revealed major differences between avirulence genes. The ndr1-1 mutation prevents hypersensitive cell death, systemic acquired resistance and PR-1 induction elicited by bacteria carrying avrRpt2. This mutation does not prevent these responses to bacteria carrying avrB. RESULTS: Systemic acquired resistance, PR-1 induction and PR-5 induction were assessed in comparisons of npr1-2 and ndr1-1 mutant plants, double mutant plants, and wild-type plants. Systemic acquired resistance was displayed by all four plant lines in response to Pseudomonas syringae bacteria carrying avrB. PR-1 induction was partially impaired by either single mutation in response to either bacterial strain, but only fully impaired in the double mutant in response to avrRpt2. PR-5 induction was not fully impaired in any of the mutants in response to either avirulence gene. CONCLUSION: Two pathways act additively, rather than in an obligatorily synergistic fashion, to induce systemic acquired resistance, PR-1 and PR-5. One of these pathways is NPR1-independent and depends on signals associated with hypersensitive cell death. The other pathway is dependent on salicylic acid accumulation and acts through NPR1. At least two other pathways also contribute additively to PR-5 induction.  (+info)

A developmental response to pathogen infection in Arabidopsis. (3/851)

We present evidence that susceptible Arabidopsis plants accelerate their reproductive development and alter their shoot architecture in response to three different pathogen species. We infected 2-week-old Arabidopsis seedlings with two bacterial pathogens, Pseudomonas syringae and Xanthomonas campestris, and an oomycete, Peronospora parasitica. Infection with each of the three pathogens reduced time to flowering and the number of aerial branches on the primary inflorescence. In the absence of competition, P. syringae and P. parasitica infection also increased basal branch development. Flowering time and branch responses were affected by the amount of pathogen present. Large amounts of pathogen caused the most dramatic changes in the number of branches on the primary inflorescence, but small amounts of P. syringae caused the fastest flowering and the production of the most basal branches. RPS2 resistance prevented large changes in development when it prevented visible disease symptoms but not at high pathogen doses and when substantial visible hypersensitive response occurred. These experiments indicate that phylogenetically disparate pathogens cause similar changes in the development of susceptible Arabidopsis. We propose that these changes in flowering time and branch architecture constitute a general developmental response to pathogen infection that may affect tolerance of and/or resistance to disease.  (+info)

Arabidopsis sfd mutants affect plastidic lipid composition and suppress dwarfing, cell death, and the enhanced disease resistance phenotypes resulting from the deficiency of a fatty acid desaturase. (4/851)

A loss-of-function mutation in the Arabidopsis SSI2/FAB2 gene, which encodes a plastidic stearoyl-acyl-carrier protein desaturase, has pleiotropic effects. The ssi2 mutant plant is dwarf, spontaneously develops lesions containing dead cells, accumulates increased salicylic acid (SA) levels, and constitutively expresses SA-mediated, NPR1-dependent and -independent defense responses. In parallel, jasmonic acid-regulated signaling is compromised in the ssi2 mutant. In an effort to discern the involvement of lipids in the ssi2-conferred developmental and defense phenotypes, we identified suppressors of fatty acid (stearoyl) desaturase deficiency (sfd) mutants. The sfd1, sfd2, and sfd4 mutant alleles suppress the ssi2-conferred dwarfing and lesion development, the NPR1-independent expression of the PATHOGENESIS-RELATED1 (PR1) gene, and resistance to Pseudomonas syringae pv maculicola. The sfd1 and sfd4 mutant alleles also depress ssi2-conferred PR1 expression in NPR1-containing sfd1 ssi2 and sfd4 ssi2 plants. By contrast, the sfd2 ssi2 plant retains the ssi2-conferred high-level expression of PR1. In parallel with the loss of ssi2-conferred constitutive SA signaling, the ability of jasmonic acid to activate PDF1.2 expression is reinstated in the sfd1 ssi2 npr1 plant. sfd4 is a mutation in the FAD6 gene that encodes a plastidic omega6-desaturase that is involved in the synthesis of polyunsaturated fatty acid-containing lipids. Because the levels of plastid complex lipid species containing hexadecatrienoic acid are depressed in all of the sfd ssi2 npr1 plants, we propose that these lipids are involved in the manifestation of the ssi2-conferred phenotypes.  (+info)

Activation of the fatty acid alpha-dioxygenase pathway during bacterial infection of tobacco leaves. Formation of oxylipins protecting against cell death. (5/851)

A pathogen-induced oxygenase showing homology to prostaglandin endoperoxide synthases-1 and -2 was recently characterized by in vitro experiments as a fatty acid alpha-dioxygenase catalyzing formation of unstable 2(R)-hydroperoxy fatty acids. To study the activity of this enzyme under in vivo conditions and to elucidate the fate of enzymatically produced 2-hydroperoxides, leaves of tobacco were analyzed for the presence of alpha-dioxygenase-generated compounds as well as for lipoxygenase (LOX) products and free fatty acids. Low basal levels of 2-hydroxylinolenic acid (0.4 nmol/g leaves fresh weight) and 8,11,14-heptadecatrienoic acid (0.1 nmol/g) could be demonstrated. These levels increased strongly upon infection with the bacterium Pseudomonas syringae pv syringae (548 and 47 nmol/g, respectively). Transgenic tobacco plants overexpressing alpha-dioxygenase were developed, and incompatible infection of such plants led to a dramatic elevation of 2-hydroxylinolenic acid (1778 nmol/g) and 8,11,14-heptadecatrienoic acid (86 nmol/g), whereas the levels of LOX products were strongly decreased. Further analysis of oxylipins in infected leaves revealed the presence of a number of 2-hydroxy fatty acids differing with respect to chain length and degree of unsaturation as well as two new doubly oxygenated oxylipins identified as 2(R),9(S)-dihydroxy-10(E),12(Z),15(Z)-octadecatrienoic acid and 2(R),9(S)-dihydroxy-10(E),12(Z)-octadecadienoic acid. alpha-Dioxygenase-generated 2-hydroxylinolenic acid, and to a lesser extent lipoxygenase-generated 9-hydroxyoctadecatrienoic acid, exerted a tissue-protective effect in bacterially infected tobacco leaves.  (+info)

RPS4-mediated disease resistance requires the combined presence of RPS4 transcripts with full-length and truncated open reading frames. (6/851)

Arabidopsis RPS4 belongs to the Toll/interleukin-1 receptor (TIR)-nucleotide binding site (NBS)-Leu-rich repeat (LRR) class of disease resistance (R) genes. Like other family members in different plant species, RPS4 produces alternative transcripts with truncated open reading frames. The dominant alternative RPS4 transcripts are generated by retention of intron 3 or introns 2 and 3, which contain in-frame stop codons and lie downstream of the NBS-encoding exon. We analyzed the biological significance of these alternative transcripts in disease resistance by removing introns 2 and 3, either individually or in combination, from a functional RPS4-Ler (Landsberg erecta) transgene. Removal of one or both introns abolished the function of the RPS4 transgene, whereas expression was not affected. In addition, a truncated RPS4-Ler transgene encoding the putative TIR and NBS domains was not sufficient to confer resistance, suggesting that the combined presence of regular and alternative RPS4 transcripts is necessary for function. Interestingly, we observed partial resistance in transgenic lines expressing both intron-deficient and truncated transgenes. This finding confirms the requirement for regular and alternative RPS4 transcripts and indicates that alternative transcripts function at the protein level rather than as regulatory RNAs. Together with published results on the tobacco N gene, our data suggest that the generation of alternative TIR-NBS-LRR R gene transcripts is of general biological significance across plant species.  (+info)

Conditional survival as a selection strategy to identify plant-inducible genes of Pseudomonas syringae. (7/851)

A novel strategy termed habitat-inducible rescue of survival (HIRS) was developed to identify genes of Pseudomonas syringae that are induced during growth on bean leaves. This strategy is based on the complementation of metXW, two cotranscribed genes that are necessary for methionine biosynthesis and required for survival of P. syringae on bean leaves exposed to conditions of low humidity. We constructed a promoter trap vector, pTrap, containing a promoterless version of the wild-type P. syringae metXW genes. Only with an active promoter fused to metXW on pTrap did this plasmid restore methionine prototrophy to the P. syringae metXW mutant B7MX89 and survival of this strain on bean leaves. To test this method, a partial library of P. syringae genomic DNA was constructed in pTrap and a total of 1,400 B7MX89 pTrap clones were subjected to HIRS selection on bean leaves. This resulted in the enrichment of five clones, each with a unique RsaI restriction pattern of their DNA insert. Sequence analysis of these clones revealed those P. syringae genes for which putative plant-inducible activity could be assigned. Promoter activity experiments with a gfp reporter gene revealed that these plant-inducible gene promoters had very low levels of expression in minimal medium. Based on green fluorescent protein fluorescence levels, it appears that many P. syringae genes have relatively low expression levels and that the metXW HIRS strategy is a sensitive method to detect weakly expressed P. syringae genes that are active on plants. Furthermore, we found that protected sites on the leaf surface provided a higher level of enrichment for P. syringae expressing metXW than exposed sites. Thus, the metXW HIRS strategy should lead to the identification of P. syringae genes that are expressed primarily in these areas on the leaf.  (+info)

Cytosolic HSP90 associates with and modulates the Arabidopsis RPM1 disease resistance protein. (8/851)

The Arabidopsis protein RPM1 activates disease resistance in response to Pseudomonas syringae proteins targeted to the inside of the host cell via the bacterial type III delivery system. We demonstrate that specific mutations in the ATP-binding domain of a single Arabidopsis cytosolic HSP90 isoform compromise RPM1 function. These mutations do not affect the function of related disease resistance proteins. RPM1 associates with HSP90 in plant cells. The Arabidopsis proteins RAR1 and SGT1 are required for the action of many R proteins, and display some structural similarity to HSP90 co-chaperones. Each associates with HSP90 in plant cells. Our data suggest that (i) RPM1 is an HSP90 client protein; and (ii) RAR1 and SGT1 may function independently as HSP90 cofactors. Dynamic interactions among these proteins can regulate RPM1 stability and function, perhaps similarly to the formation and regulation of animal steroid receptor complexes.  (+info)

  • Since the 1970s, P. syringae has been implicated as an atmospheric "biological ice nucleator", with airborne bacteria serving as cloud condensation nuclei. (
  • The role of taxis in P. syringae has not been well-studied, but the bacteria are thought to use chemical signals released by the plant to find their host and cause infection. (
  • Pseudomonas invades damaged tissue and produces a toxin that kills surrounding cells where the bacteria can then multiply. (
  • The response of epiphytic populations of Pseudomonas syringae and other bacteria on dry bean plants to four copper-based bactericides was evaluated. (
  • Comparative genomics with other P. syringae pathovars aims to throw light on the important mechanisms by which bacteria have evolved to infect trees. (
  • Psa motility resulted particularly enhanced in the supernatants of bacteria with a AHL-based QS system, such as Pseudomonas fluorescens , or an AHL-overproducing strain of Pseudomonas putida . (
  • In addition, a large number of bacteria and fungi, including Geotrichum candi dum , are sensitive to SR. The toxin traditionally has been isolated by treating P . syringae pv. (
  • The production of azelaic acid by P. syringae pathovars can be associated with plant-bacteria signaling. (
  • Because the infectious process of phytopathogenic bacteria differs from that of fungal pathogens, we have attempted to characterize pathogenicity, the ability of a pathogen to cause disease, using the phytopathogenic bacterium Pseudomonas syringae as a representative pathogen. (
  • Ice nucleation induced by Pseudomonas syringae that earned it the nickname the "rainmaking" or "snowmaking" bacteria - depending on the local prevailing atmospheric ambient temperature. (
  • the ice nucleating bacteria currently known - like Pseudomonas syringae - are mostly plant pathogens. (
  • In this scenario, the market for bactericidal products are constantly looking for new effective alternatives to control phytopathogenic bacteria, particularly species of the genus Pseudomonas and Xanthomonas that have a high economic impact globally. (
  • The mechanisms of P. syringae pathogenicity can be separated into several categories: ability to invade a plant, ability to overcome host resistance, biofilm formation, and production of proteins with ice-nucleating properties. (
  • Race structure and pathogenicity mechanisms in Pseudomonas syringae pv. (
  • The hrp pathogenicity island (PAI) of Pseudomonas syringae encodes a type III secretion system (TTSS) that translocates virulence proteins, called effectors, into plant cells. (
  • The P. syringae T3SS is a product of the hypersensitive response and pathogenicity ( hrp ) and hypersensitive response and conserved ( hrc ) gene cluster, which is strictly controlled by the codependent enhancer-binding proteins HrpR and HrpS. (
  • As a pathogen, P. syringae typically enters plant leaves through stomata, multiplies in the intercellular space (apoplast), and eventually produces necrotic lesions that are often surrounded by chlorotic halos ( 2 ). (
  • syringae (Pss), a disease of emerging importance on bean in South Africa, there is limited information available on potential sources and mechanisms of resistance. (
  • Unlike many diseases caused by pathovars of P. syringae, the host range of Pss is very large, ranging from Phaseolus vulgaris (common bean), through to Glycine max (soybean), Pisum sativum (pea) and Vigna unguiculata (cowpea). (
  • Four of these fragments, three from pPP6520 and one from pPP6525 of strain PP652, hybridized strongly to plasmid DNA from a closely-related pathovar, P. syringae pv. (
  • Effects of simulated acidic precipitation on the colonization and ice nucleation activity of Pseudomonas syringae pv. (
  • According to the obtained results it was concluded that both pathovars of P. syringae (syringae and morsprunorum) cause necrosis of cherry trees in Serbia. (