# | Rank | Similarity | Title + Abs. | Year | PMID |
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3 | 4 | 5 |
| 78 | 0 | 1.0000 | Bacterial non-host resistance: interactions of Arabidopsis with non-adapted Pseudomonas syringae strains. Although interactions of plants with virulent and avirulent host pathogens are under intensive study, relatively little is known about plant interactions with non-adapted pathogens and the molecular events underlying non-host resistance. Here we show that two Pseudomonas syringae strains for which Arabidopsis is a non-host plant, P. syringae pathovar (pv.) glycinea (Psg) and P. syringae pv. phaseolicola (Psp),induce salicylic acid (SA) accumulation and pathogenesis-related gene expression at inoculation sites, and that induction of these defences is largely dependent on bacterial type III secretion. The defence signalling components activated by non-adapted bacteria resemble those initiated by host pathogens, including SA, non-expressor of PR-1, non-race specific disease resistance 1, phytoalexin-deficient 4 and enhanced disease susceptibility 1. However, some differences in individual defence pathways induced by Psg and Psp exist, suggesting that for each strain, distinct sets of type III effectors are recognized by the plant. Although induction of SA-related defences occurs, it does not directly contribute to bacterial non-host resistance, because Arabidopsis mutants compromised in SA signalling and other classical defence pathways do not permit enhanced survival of Psg or Psp in leaves. The finding that numbers of non-adapted bacteria in leaf extracellular spaces rapidly decline after inoculation suggests that they fail to overcome toxic or structural defence barriers preceding SA-related responses. Consistent with this hypothesis, rapid, type III secretion system-independent upregulation of the lignin biosynthesis genes, PAL1 and BCB, which might contribute to an early induced, cell wall-based defence mechanism, occurs in response to non-adapted bacteria. Moreover, knockout of PAL1 permits increased leaf survival of non-host bacteria. In addition, different survival rates of non-adapted bacteria in leaves from Arabidopsis accessions and mutants with distinct glucosinolate composition or hydrolysis exist. Possible roles for early inducible, cell wall-based defences and the glucosinolate/myrosinase system in bacterial non-host resistance are discussed. | 2007 | 18251883 |
| 84 | 1 | 0.9995 | Two pathways act in an additive rather than obligatorily synergistic fashion to induce systemic acquired resistance and PR gene expression. 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. | 2002 | 12381270 |
| 85 | 2 | 0.9995 | Bacterial disease resistance in Arabidopsis through flagellin perception. Plants and animals recognize microbial invaders by detecting pathogen-associated molecular patterns (PAMPs) such as flagellin. However, the importance of flagellin perception for disease resistance has, until now, not been demonstrated. Here we show that treatment of plants with flg22, a peptide representing the elicitor-active epitope of flagellin, induces the expression of numerous defence-related genes and triggers resistance to pathogenic bacteria in wild-type plants, but not in plants carrying mutations in the flagellin receptor gene FLS2. This induced resistance seems to be independent of salicylic acid, jasmonic acid and ethylene signalling. Wild-type and fls2 mutants both display enhanced resistance when treated with crude bacterial extracts, even devoid of elicitor-active flagellin, indicating the existence of functional perception systems for PAMPs other than flagellin. Although fls2 mutant plants are as susceptible as the wild type when bacteria are infiltrated into leaves, they are more susceptible to the pathogen Pseudomonas syringae pv. tomato DC3000 when it is sprayed on the leaf surface. Thus, flagellin perception restricts bacterial invasion, probably at an early step, and contributes to the plant's disease resistance. | 2004 | 15085136 |
| 8776 | 3 | 0.9995 | Systemic resistance induced by rhizosphere bacteria. Nonpathogenic rhizobacteria can induce a systemic resistance in plants that is phenotypically similar to pathogen-induced systemic acquired resistance (SAR). Rhizobacteria-mediated induced systemic resistance (ISR) has been demonstrated against fungi, bacteria, and viruses in Arabidopsis, bean, carnation, cucumber, radish, tobacco, and tomato under conditions in which the inducing bacteria and the challenging pathogen remained spatially separated. Bacterial strains differ in their ability to induce resistance in different plant species, and plants show variation in the expression of ISR upon induction by specific bacterial strains. Bacterial determinants of ISR include lipopolysaccharides, siderophores, and salicylic acid (SA). Whereas some of the rhizobacteria induce resistance through the SA-dependent SAR pathway, others do not and require jasmonic acid and ethylene perception by the plant for ISR to develop. No consistent host plant alterations are associated with the induced state, but upon challenge inoculation, resistance responses are accelerated and enhanced. ISR is effective under field conditions and offers a natural mechanism for biological control of plant disease. | 1998 | 15012509 |
| 83 | 4 | 0.9995 | Transcriptional responses of Arabidopsis thaliana to the bacteria-derived PAMPs harpin and lipopolysaccharide. Many plant-pathogen interactions are controlled by specific interactions between pathogen avirulence (avr) gene loci and the corresponding plant resistance R locus (gene-for-gene-hypothesis). Very often, this type of interaction culminates in a hypersensitive reaction (HR). However, recently pathogen-associated molecular patterns (PAMPs) such as flagellin or lipopolysaccharides (LPS) that are common to all bacteria have been shown to act as general elicitors of basal or innate immune responses in several plant species. Here, we summarize the genetic programs in Arabidopsis thaliana behind the LPS-induced basal response and the HR induced by harpin, respectively. Using Agilent Arabidopsis cDNA microarrays consisting of approximately 15,000 oligomers, changes in transcript accumulation of treated cells were monitored over a period of 24h after elicitor treatment. Analysis of the array data revealed significant responses to LPS (309 genes), harpin (951 genes) or both (313 genes). Concentrating our analysis on the genes encoding transcription factors, defence genes, cell wall biogenesis-related genes and signal transduction components we monitored interesting parallels, but also remarkably different expression patterns. Harpin and LPS induced an overlapping set of genes involved in cell wall biogenesis, cellular communication and signalling. The pattern of induced genes associated with cell rescue and general stress responses such as small heat-shock proteins was highly similar. In contrast, there is a striking difference regarding some of the most prominent, central components of plant defence such as WRKY transcription factors and oxidative burst-associated genes like NADPH oxidases, whose expression became apparent only after treatment with harpin. While both harpin and LPS can stimulate plant immunity in Arabidopsis, the PAMP LPS induces much more subtle host reactions at the transcriptome scale. The defence machinery induced by harpin resembles the known HR-type host responses leading to cell death after treatment with this elicitor. LPS is a weak inducer of basal resistance and induces a different pattern of genes. Strikingly the biggest overlap (40) of responding genes was found between the early harpin response (30min) and the late LPS response (24h). | 2008 | 18406364 |
| 8777 | 5 | 0.9995 | Systemic resistance in Arabidopsis induced by biocontrol bacteria is independent of salicylic acid accumulation and pathogenesis-related gene expression. Systemic acquired resistance is a pathogen-inducible defense mechanism in plants. The resistant state is dependent on endogenous accumulation of salicylic acid (SA) and is characterized by the activation of genes encoding pathogenesis-related (PR) proteins. Recently, selected nonpathogenic, root-colonizing biocontrol bacteria have been shown to trigger a systemic resistance response as well. To study the molecular basis underlying this type of systemic resistance, we developed an Arabidopsis-based model system using Fusarium oxysporum f sp raphani and Pseudomonas syringae pv tomato as challenging pathogens. Colonization of the rhizosphere by the biological control strain WCS417r of P. fluorescens resulted in a plant-mediated resistance response that significantly reduced symptoms elicited by both challenging pathogens. Moreover, growth of P. syringae in infected leaves was strongly inhibited in P. fluorescens WCS417r-treated plants. Transgenic Arabidopsis NahG plants, unable to accumulate SA, and wild-type plants were equally responsive to P. fluorescens WCS417r-mediated induction of resistance. Furthermore, P. fluorescens WCS417r-mediated systemic resistance did not coincide with the accumulation of PR mRNAs before challenge inoculation. These results indicate that P. fluorescens WCS417r induces a pathway different from the one that controls classic systemic acquired resistance and that this pathway leads to a form of systemic resistance independent of SA accumulation and PR gene expression. | 1996 | 8776893 |
| 86 | 6 | 0.9994 | Decreased abundance of type III secretion system-inducing signals in Arabidopsis mkp1 enhances resistance against Pseudomonas syringae. Genes encoding the virulence-promoting type III secretion system (T3SS) in phytopathogenic bacteria are induced at the start of infection, indicating that recognition of signals from the host plant initiates this response. However, the precise nature of these signals and whether their concentrations can be altered to affect the biological outcome of host-pathogen interactions remain speculative. Here we use a metabolomic comparison of resistant and susceptible genotypes to identify plant-derived metabolites that induce T3SS genes in Pseudomonas syringae pv tomato DC3000 and report that mapk phosphatase 1 (mkp1), an Arabidopsis mutant that is more resistant to bacterial infection, produces decreased levels of these bioactive compounds. Consistent with these observations, T3SS effector expression and delivery by DC3000 was impaired when infecting the mkp1 mutant. The addition of bioactive metabolites fully restored T3SS effector delivery and suppressed the enhanced resistance in the mkp1 mutant. Pretreatment of plants with pathogen-associated molecular patterns (PAMPs) to induce PAMP-triggered immunity (PTI) also restricts T3SS effector delivery and enhances resistance by unknown mechanisms, and the addition of the bioactive metabolites similarly suppressed both aspects of PTI. Together, these results demonstrate that DC3000 perceives multiple signals derived from plants to initiate its T3SS and that the level of these host-derived signals impacts bacterial pathogenesis. | 2014 | 24753604 |
| 80 | 7 | 0.9994 | Virus infection induces resistance to Pseudomonas syringae and to drought in both compatible and incompatible bacteria-host interactions, which are compromised under conditions of elevated temperature and CO(2) levels. Plants are simultaneously exposed to a variety of biotic and abiotic stresses, such as infections by viruses and bacteria, or drought. This study aimed to improve our understanding of interactions between viral and bacterial pathogens and the environment in the incompatible host Nicotiana benthamiana and the susceptible host Arabidopsis thaliana, and the contribution of viral virulence proteins to these responses. Infection by the Potato virus X (PVX)/Plum pox virus (PPV) pathosystem induced resistance to Pseudomonas syringae (Pst) and to drought in both compatible and incompatible bacteria-host interactions, once a threshold level of defence responses was triggered by the virulence proteins P25 of PVX and the helper component proteinase of PPV. Virus-induced resistance to Pst was compromised in salicylic acid and jasmonic acid signalling-deficient Arabidopsis but not in N. benthamiana lines. Elevated temperature and CO(2) levels, parameters associated with climate change, negatively affected resistance to Pst and to drought induced by virus infection, and this correlated with diminished H(2)O(2) production, decreased expression of defence genes and a drop in virus titres. Thus, diminished virulence should be considered as a potential factor limiting the outcome of beneficial trade-offs in the response of virus-infected plants to drought or bacterial pathogens under a climate change scenario. | 2020 | 31730035 |
| 8778 | 8 | 0.9994 | The transcriptome of rhizobacteria-induced systemic resistance in arabidopsis. Plants develop an enhanced defensive capacity against a broad spectrum of plant pathogens after colonization of the roots by selected strains of nonpathogenic, fluorescent Pseudomonas spp. In Arabidopsis thaliana, this rhizobacteria-induced systemic resistance (ISR) functions independently of salicylic acid but requires responsiveness to the plant hormones jasmonic acid and ethylene. In contrast to pathogen-induced systemic acquired resistance, rhizobacteria-mediated ISR is not associated with changes in the expression of genes encoding pathogenesis-related proteins. To identify ISR-related genes, we surveyed the transcriptional response of over 8,000 Arabidopsis genes during rhizobacteria-mediated ISR. Locally in the roots, ISR-inducing Pseudomonas fluorescens WCS417r bacteria elicited a substantial change in the expression of 97 genes. However, systemically in the leaves, none of the approximately 8,000 genes tested showed a consistent change in expression in response to effective colonization of the roots by WCS417r, indicating that the onset of ISR in the leaves is not associated with detectable changes in gene expression. After challenge inoculation of WCS417r-induced plants with the bacterial leaf pathogen P. syringae pv. tomato DC3000, 81 genes showed an augmented expression pattern in ISR-expressing leaves, suggesting that these genes were primed to respond faster or more strongly upon pathogen attack. The majority of the primed genes was predicted to be regulated by jasmonic acid or ethylene signaling. Priming of pathogen-induced genes allows the plant to react more effectively to the invader encountered, which might explain the broad-spectrum action of rhizobacteria-mediated ISR. | 2004 | 15305611 |
| 89 | 9 | 0.9993 | The Arabidopsis flavin-dependent monooxygenase FMO1 is an essential component of biologically induced systemic acquired resistance. Upon localized attack by necrotizing pathogens, plants gradually develop increased resistance against subsequent infections at the whole-plant level, a phenomenon known as systemic acquired resistance (SAR). To identify genes involved in the establishment of SAR, we pursued a strategy that combined gene expression information from microarray data with pathological characterization of selected Arabidopsis (Arabidopsis thaliana) T-DNA insertion lines. A gene that is up-regulated in Arabidopsis leaves inoculated with avirulent or virulent strains of the bacterial pathogen Pseudomonas syringae pv maculicola (Psm) showed homology to flavin-dependent monooxygenases (FMO) and was designated as FMO1. An Arabidopsis knockout line of FMO1 proved to be fully impaired in the establishment of SAR triggered by avirulent (Psm avrRpm1) or virulent (Psm) bacteria. Loss of SAR in the fmo1 mutants was accompanied by the inability to initiate systemic accumulation of salicylic acid (SA) and systemic expression of diverse defense-related genes. In contrast, responses at the site of pathogen attack, including increases in the levels of the defense signals SA and jasmonic acid, camalexin accumulation, and expression of various defense genes, were induced in a similar manner in both fmo1 mutant and wild-type plants. Consistently, the fmo1 mutation did not significantly affect local disease resistance toward virulent or avirulent bacteria in naive plants. Induction of FMO1 expression at the site of pathogen inoculation is independent of SA signaling, but attenuated in the Arabidopsis eds1 and pad4 defense mutants. Importantly, FMO1 expression is also systemically induced upon localized P. syringae infection. This systemic up-regulation is missing in the SAR-defective SA pathway mutants sid2 and npr1, as well as in the defense mutant ndr1, indicating a close correlation between systemic FMO1 expression and SAR establishment. Our findings suggest that the presence of the FMO1 gene product in systemic tissue is critical for the development of SAR, possibly by synthesis of a metabolite required for the transduction or amplification of a signal during the early phases of SAR establishment in systemic leaves. | 2006 | 16778014 |
| 8150 | 10 | 0.9993 | ROS production during symbiotic infection suppresses pathogenesis-related gene expression. Leguminous plants have exclusive ability to form symbiotic relationship with soil bacteria of the genus Rhizobium. Symbiosis is a complex process that involves multiple molecular signaling activities, such as calcium fluxes, production of reactive oxygen species (ROS) and synthesis of nodulation genes. We analyzed the role of ROS in defense gene expression in Medicago truncatula during symbiosis and pathogenesis. Studies in Arabidopsis thaliana showed that the induction of pathogenesis-related (PR) genes during systemic acquired resistance (SAR) is regulated by NPR1 protein, which resides in the cytoplasm as an oligomer. After oxidative burst and return of reducing conditions, the NPR1 undergoes monomerization and becomes translocated to the nucleus, where it functions in PR genes induction. We show that ROS production is both stronger and longer during symbiotic interactions than during interactions with pathogenic, nonhost or common nonpathogenic soil bacteria. Moreover, root cells inoculated with Sinorhizobium meliloti accumulated ROS in the cytosol but not in vacuoles, as opposed to Pseudomonas putida inoculation or salt stress treatment. Furthermore, increased ROS accumulation by addition of H₂O₂ reduced the PR gene expression, while catalase had an opposite effect, establishing that the PR gene expression is opposite to the level of cytoplasmic ROS. In addition, we show that salicylic acid pretreatment significantly reduced ROS production in root cells during symbiotic interaction. | 2012 | 22499208 |
| 8315 | 11 | 0.9993 | The Induction and Modulation of Plant Defense Responses by Bacterial Lipopolysaccharides. Lipopolysaccharides (LPSs) are ubiquitous, indispensable components of the cell surface of Gram-negative bacteria that apparently have diverse roles in bacterial pathogenesis of plants. As an outer membrane component, LPS may contribute to the exclusion of plant-derived antimicrobial compounds promoting the ability of a bacterial plant pathogen to infect plants. In contrast, LPS can be recognized by plants to directly trigger some plant defense-related responses. LPS can also alter the response of plants to subsequent bacterial inoculation; these delayed effects include alterations in the expression patterns of genes coding for some pathogenesis-related (PR) proteins, promotion of the synthesis of antimicrobial hydroxycinnamoyl-tyramine conjugates, and prevention of the hypersensitive reaction caused by avirulent bacteria. Prevention of the response may allow expression of resistance in the absence of catastrophic tissue damage. Recognition of LPS (and other nonspecific determinants) may initiate responses in plants that restrict the growth of nonpathogenic bacteria, whereas plant pathogens may possess hrp gene-dependent mechanisms to suppress such responses. | 2000 | 11701843 |
| 81 | 12 | 0.9993 | Biological control of bacterial wilt in Arabidopsis thaliana involves abscissic acid signalling. Means to control bacterial wilt caused by the phytopathogenic root bacteria Ralstonia solanacearum are limited. Mutants in a large cluster of genes (hrp) involved in the pathogenicity of R. solanacearum were successfully used in a previous study as endophytic biocontrol agents in challenge inoculation experiments on tomato. However, the molecular mechanisms controlling this resistance remained unknown. We developed a protection assay using Arabidopsis thaliana as a model plant and analyzed the events underlying the biological control by genetic, transcriptomic and molecular approaches. High protection rates associated with a significant decrease in the multiplication of R. solanacearum were observed in plants pre-inoculated with a ΔhrpB mutant strain. Neither salicylic acid, nor jasmonic acid/ethylene played a role in the establishment of this resistance. Microarray analysis showed that 26% of the up-regulated genes in protected plants are involved in the biosynthesis and signalling of abscissic acid (ABA). In addition 21% of these genes are constitutively expressed in the irregular xylem cellulose synthase mutants (irx), which present a high level of resistance to R. solanacearum. We propose that inoculation with the ΔhrpB mutant strain generates a hostile environment for subsequent plant colonization by a virulent strain of R. solanacearum. | 2012 | 22432714 |
| 325 | 13 | 0.9993 | Use of Arabidopsis thaliana and Pseudomonas syringae in the Study of Plant Disease Resistance and Tolerance. The interaction between Arabidopsis thaliana and the bacterium Pseudomonas syringae is being developed as a model experimental system for plant pathology research. Race-specific ("gene-for-gene") resistance has been demonstrated for this interaction, and pathogen genes that determine avirulence have been isolated and characterized. Because certain lines of both Arabidopsis and soybean are resistant to bacteria carrying the avirulence genes avrRpt2 and avrB, extremely similar pathogen recognition mechanisms are apparently present in these two plant species. Isogenic bacterial strains that differ by the presence of single avirulence genes are being used to analyze plant resistance. Plant resistance genes have been identified in crosses between resistant and susceptible lines. The extensive map-based cloning tools available in Arabidopsis are being used to isolate these resistance genes. In a related project, ethylene-insensitive Arabidopsis mutants are being used to examine the role of ethylene in disease development. Ethylene apparently mediates symptom formation in susceptible plants and is not required for resistance, suggesting possible strategies for enhancement of disease tolerance in crops. | 1993 | 19279805 |
| 82 | 14 | 0.9992 | Type III effectors orchestrate a complex interplay between transcriptional networks to modify basal defence responses during pathogenesis and resistance. To successfully infect a plant, bacterial pathogens inject a collection of Type III effector proteins (TTEs) directly into the plant cell that function to overcome basal defences and redirect host metabolism for nutrition and growth. We examined (i) the transcriptional dynamics of basal defence responses between Arabidopsis thaliana and Pseudomonas syringae and (ii) how basal defence is subsequently modulated by virulence factors during compatible interactions. A set of 96 genes displaying an early, sustained induction during basal defence was identified. These were also universally co-regulated following other bacterial basal resistance and non-host responses or following elicitor challenges. Eight hundred and eighty genes were conservatively identified as being modulated by TTEs within 12 h post-inoculation (hpi), 20% of which represented transcripts previously induced by the bacteria at 2 hpi. Significant over-representation of co-regulated transcripts encoding leucine rich repeat receptor proteins and protein phosphatases were, respectively, suppressed and induced 12 hpi. These data support a model in which the pathogen avoids detection through diminution of extracellular receptors and attenuation of kinase signalling pathways. Transcripts associated with several metabolic pathways, particularly plastid based primary carbon metabolism, pigment biosynthesis and aromatic amino acid metabolism, were significantly modified by the bacterial challenge at 12 hpi. Superimposed upon this basal response, virulence factors (most likely TTEs) targeted genes involved in phenylpropanoid biosynthesis, consistent with the abrogation of lignin deposition and other wall modifications likely to restrict the passage of nutrients and water to the invading bacteria. In contrast, some pathways associated with stress tolerance are transcriptionally induced at 12 hpi by TTEs. | 2006 | 16553893 |
| 79 | 15 | 0.9992 | A novel link between tomato GRAS genes, plant disease resistance and mechanical stress response. SUMMARY Members of the GRAS family of transcriptional regulators have been implicated in the control of plant growth and development, and in the interaction of plants with symbiotic bacteria. Here we examine the complexity of the GRAS gene family in tomato (Solanum lycopersicum) and investigate its role in disease resistance and mechanical stress. A large number of tomato ESTs corresponding to GRAS transcripts were retrieved from the public database and assembled in 17 contigs of putative genes. Expression analysis of these genes by real-time RT-PCR revealed that six SlGRAS transcripts accumulate during the onset of disease resistance to Pseudomonas syringae pv. tomato. Further analysis of two selected family members showed that their transcripts preferentially accumulate in tomato plants in response to different avirulent bacteria or to the fungal elicitor EIX, and their expression kinetics correlate with the appearance of the hypersensitive response. In addition, transcript levels of eight SlGRAS genes, including all the Pseudomonas-inducible family members, increased in response to mechanical stress much earlier than upon pathogen attack. Accumulation of SlGRAS transcripts following mechanical stress was in part dependent on the signalling molecule jasmonic acid. Remarkably, suppression of SlGRAS6 gene expression by virus-induced gene silencing impaired tomato resistance to P. syringae pv. tomato. These results support a function for GRAS transcriptional regulators in the plant response to biotic and abiotic stress. | 2006 | 20507472 |
| 327 | 16 | 0.9992 | Natural variation in RPS2-mediated resistance among Arabidopsis accessions: correlation between gene expression profiles and phenotypic responses. Natural variation in gene expression (expression traits or e-traits) is increasingly used for the discovery of genes controlling traits. An important question is whether a particular e-trait is correlated with a phenotypic trait. Here, we examined the correlations between phenotypic traits and e-traits among 10 Arabidopsis thaliana accessions. We studied defense against Pseudomonas syringae pv tomato DC3000 (Pst), with a focus on resistance gene-mediated resistance triggered by the type III effector protein AvrRpt2. As phenotypic traits, we measured growth of the bacteria and extent of the hypersensitive response (HR) as measured by electrolyte leakage. Genetic variation among accessions affected growth of Pst both with (Pst avrRpt2) and without (Pst) the AvrRpt2 effector. Variation in HR was not correlated with variation in bacterial growth. We also collected gene expression profiles 6 h after mock and Pst avrRpt2 inoculation using a custom microarray. Clusters of genes whose expression levels are correlated with bacterial growth or electrolyte leakage were identified. Thus, we demonstrated that variation in gene expression profiles of Arabidopsis accessions collected at one time point under one experimental condition has the power to explain variation in phenotypic responses to pathogen attack. | 2007 | 18083910 |
| 77 | 17 | 0.9992 | A pathogen-inducible patatin-like lipid acyl hydrolase facilitates fungal and bacterial host colonization in Arabidopsis. Genes and proteins related to patatin, the major storage protein of potato tubers, have been identified in many plant species and shown to be induced by a variety of environmental stresses. The Arabidopsis patatin-like gene family (PLPs) comprises nine members, two of which (PLP2 and PLP7) are strongly induced in leaves challenged with fungal and bacterial pathogens. Here we show that accumulation of PLP2 protein in response to Botrytis cinerea or Pseudomonas syringae pv. tomato (avrRpt2) is dependent on jasmonic acid and ethylene signaling, but is not dependent on salicylic acid. Expression of a PLP2-green fluorescent protein (GFP) fusion protein and analysis of recombinant PLP2 indicates that PLP2 encodes a cytoplasmic lipid acyl hydrolase with wide substrate specificity. Transgenic plants with altered levels of PLP2 protein were generated and assayed for pathogen resistance. Plants silenced for PLP2 expression displayed enhanced resistance to B. cinerea, whereas plants overexpressing PLP2 were much more sensitive to this necrotrophic fungus. We also established a positive correlation between the level of PLP2 expression in transgenic plants and cell death or damage in response to paraquat treatment or infection by avirulent P. syringae. Interestingly, repression of PLP2 expression increased resistance to avirulent bacteria, while PLP2-overexpressing plants multiplied avirulent bacteria close to the titers reached by virulent bacteria. Collectively, the data indicate that PLP2-encoded lipolytic activity can be exploited by pathogens with different lifestyles to facilitate host colonization. In particular PLP2 potentiates plant cell death inflicted by Botrytis and reduces the efficiency of the hypersensitive response in restricting the multiplication of avirulent bacteria. Both effects are possibly mediated by providing fatty acid precursors of bioactive oxylipins. | 2005 | 16297072 |
| 8151 | 18 | 0.9992 | Azospirillum: benefits that go far beyond biological nitrogen fixation. The genus Azospirillum comprises plant-growth-promoting bacteria (PGPB), which have been broadly studied. The benefits to plants by inoculation with Azospirillum have been primarily attributed to its capacity to fix atmospheric nitrogen, but also to its capacity to synthesize phytohormones, in particular indole-3-acetic acid. Recently, an increasing number of studies has attributed an important role of Azospirillum in conferring to plants tolerance of abiotic and biotic stresses, which may be mediated by phytohormones acting as signaling molecules. Tolerance of biotic stresses is controlled by mechanisms of induced systemic resistance, mediated by increased levels of phytohormones in the jasmonic acid/ethylene pathway, independent of salicylic acid (SA), whereas in the systemic acquired resistance-a mechanism previously studied with phytopathogens-it is controlled by intermediate levels of SA. Both mechanisms are related to the NPR1 protein, acting as a co-activator in the induction of defense genes. Azospirillum can also promote plant growth by mechanisms of tolerance of abiotic stresses, named as induced systemic tolerance, mediated by antioxidants, osmotic adjustment, production of phytohormones, and defense strategies such as the expression of pathogenesis-related genes. The study of the mechanisms triggered by Azospirillum in plants can help in the search for more-sustainable agricultural practices and possibly reveal the use of PGPB as a major strategy to mitigate the effects of biotic and abiotic stresses on agricultural productivity. | 2018 | 29728787 |
| 326 | 19 | 0.9992 | Quantitative nature of Arabidopsis responses during compatible and incompatible interactions with the bacterial pathogen Pseudomonas syringae. We performed large-scale mRNA expression profiling using an Affymetrix GeneChip to study Arabidopsis responses to the bacterial pathogen Pseudomonas syringae. The interactions were compatible (virulent bacteria) or incompatible (avirulent bacteria), including a nonhost interaction and interactions mediated by two different avirulence gene-resistance (R) gene combinations. Approximately 2000 of the approximately 8000 genes monitored showed reproducible significant expression level changes in at least one of the interactions. Analysis of biological variation suggested that the system behavior of the plant response in an incompatible interaction was robust but that of a compatible interaction was not. A large part of the difference between incompatible and compatible interactions can be explained quantitatively. Despite high similarity between responses mediated by the R genes RPS2 and RPM1 in wild-type plants, RPS2-mediated responses were strongly suppressed by the ndr1 mutation and the NahG transgene, whereas RPM1-mediated responses were not. This finding is consistent with the resistance phenotypes of these plants. We propose a simple quantitative model with a saturating response curve that approximates the overall behavior of this plant-pathogen system. | 2003 | 12566575 |