Correction: Autoacetylation of the Ralstonia solanacearum Effector PopP2 Targets a Lysine Residue Essential for RRS1-R-Mediated Immunity in Arabidopsis.

[This corrects the article DOI: 10.1371/journal.ppat.

Arabidopsis CLAVATA1 and CLAVATA2 receptors contribute to Ralstonia solanacearum pathogenicity through a miR169-dependent pathway.

Bacterial wilt caused by Ralstonia solanacearum is one of the most destructive bacterial plant diseases. Although many molecular determinants involved in R. solanacearum adaptation to hosts and pathogenesis have been described, host components required for disease establishment remain poorly characterized.

Evolutionarily distant pathogens require the Arabidopsis phytosulfokine signalling pathway to establish disease.

Secreted peptides and their specific receptors frequently orchestrate cell-to-cell communication in plants. Phytosulfokines (PSKs) are secreted tyrosine-sulphated peptide hormones, which trigger cellular dedifferentiation and redifferentiation upon binding to their membrane receptor. Biotrophic plant pathogens frequently trigger the differentiation of host cells into specialized feeding structures, which are essential for successful infection.

The receptor kinase IMPAIRED OOMYCETE SUSCEPTIBILITY1 attenuates abscisic acid responses in Arabidopsis.

In plants, membrane-bound receptor kinases are essential for developmental processes, immune responses to pathogens and the establishment of symbiosis. We previously identified the Arabidopsis (Arabidopsis thaliana) receptor kinase IMPAIRED OOMYCETE SUSCEPTIBILITY1 (IOS1) as required for successful infection with the downy mildew pathogen Hyaloperonospora arabidopsidis. We report here that IOS1 is also required for full susceptibility of Arabidopsis to unrelated (hemi)biotrophic filamentous oomycete and fungal pathogens.

The Brassicaceae-specific EWR1 gene provides resistance to vascular wilt pathogens.

Soil-borne vascular wilt diseases caused by Verticillium spp. are among the most destructive diseases worldwide in a wide range of plant species. The most effective means of controlling Verticillium wilt diseases is the use of genetic resistance.

Hrp mutant bacteria as biocontrol agents: toward a sustainable approach in the fight against plant pathogenic bacteria.

Sustainable agriculture necessitates development of environmentally safe methods to protect plants against pathogens. Among these methods, application of biocontrol agents has been efficiently used to minimize disease development. Here we review current understanding of mechanisms involved in biocontrol of the main Gram-phytopathogenic bacteria-induced diseases by plant inoculation with strains mutated in hrp (hypersensitive response and pathogenicity) genes.

Gene-for-gene tolerance to bacterial wilt in Arabidopsis.

Bacterial wilt caused by Ralstonia solanacearum is a disease of widespread economic importance that affects numerous plant species, including Arabidopsis thaliana. We describe a pathosystem between A. thaliana and biovar 3 phylotype I strain BCCF402 of R.

Arabidopsis wat1 (walls are thin1)-mediated resistance to the bacterial vascular pathogen, Ralstonia solanacearum, is accompanied by cross-regulation of salicylic acid and tryptophan metabolism.

Inactivation of Arabidopsis WAT1 (Walls Are Thin1), a gene required for secondary cell-wall deposition, conferred broad-spectrum resistance to vascular pathogens, including the bacteria Ralstonia solanacearum and Xanthomonas campestris pv. campestris, and the fungi Verticillium dahliae and Verticillium albo-atrum. Introduction of NahG, the bacterial salicylic acid (SA)-degrading salicylate hydroxylase gene, into the wat1 mutant restored full susceptibility to both R.

Deciphering the route of Ralstonia solanacearum colonization in Arabidopsis thaliana roots during a compatible interaction: focus at the plant cell wall.

The compatible interaction between the model plant, Arabidopsis thaliana, and the GMI1000 strain of the phytopathogenic bacterium, Ralstonia solanacearum, was investigated in an in vitro pathosystem. We describe the progression of the bacteria in the root from penetration at the root surface to the xylem vessels and the cell type-specific, cell wall-associated modifications that accompanies bacterial colonization. Within 6 days post inoculation, R.

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.

The Arabidopsis thaliana DNA-binding protein AHL19 mediates verticillium wilt resistance.

Verticillium spp. are destructive soilborne fungal pathogens that cause vascular wilt diseases in a wide range of plant species. Verticillium wilts are particularly notorious, and genetic resistance in crop plants is the most favorable means of disease control.

Autoacetylation of the Ralstonia solanacearum effector PopP2 targets a lysine residue essential for RRS1-R-mediated immunity in Arabidopsis.

Type III effector proteins from bacterial pathogens manipulate components of host immunity to suppress defence responses and promote pathogen development. In plants, host proteins targeted by some effectors called avirulence proteins are surveyed by plant disease resistance proteins referred to as "guards". The Ralstonia solanacearum effector protein PopP2 triggers immunity in Arabidopsis following its perception by the RRS1-R resistance protein.

The ERECTA Receptor-Like Kinase Regulates Cell Wall-Mediated Resistance to Pathogens in Arabidopsis thaliana.

Some receptor-like kinases (RLK) control plant development while others regulate immunity. The Arabidopsis ERECTA (ER) RLK regulates both biological processes. To discover specific components of ER-mediated immunity, a genetic screen was conducted to identify suppressors of erecta (ser) susceptibility to Plectosphaerella cucumerina fungus.

Delayed Symptom Development in ein2-1, an Arabidopsis Ethylene-Insensitive Mutant, in Response to Bacterial Wilt Caused by Ralstonia solanacearum.

ABSTRACT Wilt disease caused by the phytopathogenic bacterium Ralstonia solanacearum is poorly understood at the molecular level. The possible roles of salicylic acid, jasmonic acid, and ethylene, compounds commonly associated with the plant response to pathogens, in wilt symptom development were investigated using various Arabidopsis thaliana mutants in a Col-0 background, an ecotype that develops wilt symptoms in response to the virulent GMI1000 strain. Following root inoculation, wilt symptoms were delayed in ein2-1, an ethylene-insensitive mutant, in response to several virulent strains of the pathogen.

Isolation and Characterization of a Novel Arabidopsis thaliana Mutant Unable to Develop Wilt Symptoms After Inoculation with a Virulent Strain of Ralstonia solanacearum.

ABSTRACT To characterize host genes required for a compatible interaction, we identified a novel recessive Arabidopsis thaliana mutant, nws1 (no wilt symptoms), that failed to develop wilt symptoms in response to virulent strains of the phytopathogenic bacterium, Ralstonia solanacearum. The absence of wilting in nws1 plants was not correlated with a cell death phenotype or a constitutive expression of salicylic acid-, jasmonic acid- or ethylene-associated genes. In addition, this mutation, which conferred a symptomless phenotype in response to all the R.

RD19, an Arabidopsis cysteine protease required for RRS1-R-mediated resistance, is relocalized to the nucleus by the Ralstonia solanacearum PopP2 effector.

Bacterial wilt, a disease impacting cultivated crops worldwide, is caused by the pathogenic bacterium Ralstonia solanacearum. PopP2 (for Pseudomonas outer protein P2) is an R. solanacearum type III effector that belongs to the YopJ/AvrRxv protein family and interacts with the Arabidopsis thaliana RESISTANT TO RALSTONIA SOLANACEARUM 1-R (RRS1-R) resistance protein.

The Arabidopsis transcription factor WRKY27 influences wilt disease symptom development caused by Ralstonia solanacearum.

WRKY transcription factors play a key role in modulating the plant defense transcriptome. Here we show that the Arabidopsis mutant wrky27-1, which lacks a functional WRKY27 transcription factor, showed delayed symptom development in response to the bacterial wilt pathogen Ralstonia solanacearum. Additionally, wrky27-1 plants did not express PR marker genes upon infection, as also observed in resistant Nd-1 plants.

Transcriptional responses of Arabidopsis thaliana during wilt disease caused by the soil-borne phytopathogenic bacterium, Ralstonia solanacearum.

Bacterial wilt is a common disease that causes severe yield and quality losses in many plants. In the present study, we used the model Ralstonia solanacearum-Arabidopsis thaliana pathosystem to study transcriptional changes associated with wilt disease development. Susceptible Col-5 plants and RRS1-R-containing resistant Nd-1 plants were root-inoculated with R.

Impairment of cellulose synthases required for Arabidopsis secondary cell wall formation enhances disease resistance.

Cellulose is synthesized by cellulose synthases (CESAs) contained in plasma membrane-localized complexes. In Arabidopsis thaliana, three types of CESA subunits (CESA4/IRREGULAR XYLEM5 [IRX5], CESA7/IRX3, and CESA8/IRX1) are required for secondary cell wall formation. We report that mutations in these proteins conferred enhanced resistance to the soil-borne bacterium Ralstonia solanacearum and the necrotrophic fungus Plectosphaerella cucumerina.

A single amino acid insertion in the WRKY domain of the Arabidopsis TIR-NBS-LRR-WRKY-type disease resistance protein SLH1 (sensitive to low humidity 1) causes activation of defense responses and hypersensitive cell death.

In this study we characterized the sensitive to low humidity 1 (slh1) mutant of Arabidopsis ecotype No-0 which exhibits normal growth on agar plate medium but which on transfer to soil shows growth arrest and development of necrotic lesions. cDNA microarray hybridization and RNA gel blot analysis revealed that genes associated with activation of disease resistance were upregulated in the slh1 mutants in response to conditions of low humidity. Furthermore, the slh1 mutants accumulate callose, autofluorescent compounds and salicylic acid (SA).

The Arabidopsis cytosolic thioredoxin h5 gene induction by oxidative stress and its W-box-mediated response to pathogen elicitor.

The AtTRXh5 protein belongs to the cytosolic thioredoxins h family that, in Arabidopsis, contains eight members showing very distinct patterns and levels of expression. Here, we show that the AtTRXh5 gene is up-regulated during wounding, abscission, and senescence, as well as during incompatible interactions with the bacterial pathogen Pseudomonas syringae. By electrophoretic mobility shift assays, a binding activity on a W-box in the AtTRXh5 promoter region was found induced by treatments with the P.

ERECTA, an LRR receptor-like kinase protein controlling development pleiotropically affects resistance to bacterial wilt.

Bacterial wilt, one of the most devastating bacterial diseases of plants worldwide, is caused by Ralstonia solanacearum and affects many important crop species. We show that several strains isolated from solanaceous crops in Europe are pathogenic in different accessions of Arabidopsis thaliana. One of these strains, 14.

Physical interaction between RRS1-R, a protein conferring resistance to bacterial wilt, and PopP2, a type III effector targeted to the plant nucleus.

RRS1-R confers broad-spectrum resistance to several strains of the causal agent of bacterial wilt, Ralstonia solanacearum. Although genetically defined as recessive, this R gene encodes a protein whose structure combines the TIR-NBS-LRR domains found in several R proteins and a WRKY motif characteristic of some plant transcriptional factors and behaves as a dominant gene in transgenic susceptible plants. Here we show that PopP2, a R.

Resistance to Ralstonia solanacearum in Arabidopsis thaliana is conferred by the recessive RRS1-R gene, a member of a novel family of resistance genes.

The identification of two Arabidopsis thaliana genes involved in determining recessive resistance to several strains of the causal agent of bacterial wilt, Ralstonia solanacearum, is reported. Dominant (RRS1-S) and recessive (RRS1-R) alleles from susceptible and resistant accessions encode highly similar predicted proteins differing in length and which present a novel structure combining domains found in plant Toll-IL-1 receptor-nucleotide binding site-leucin-rich repeat resistance proteins and a WRKY motif characteristic of some plant transcriptional factors. Although genetically defined as a recessive allele, RRS1-R behaves as a dominant resistance gene in transgenic plants.