RESUMO
Since 2005, the Pathogen-Host Interactions Database (PHI-base) has manually curated experimentally verified pathogenicity, virulence and effector genes from fungal, bacterial and protist pathogens, which infect animal, plant, fish, insect and/or fungal hosts. PHI-base (www.phi-base.org) is devoted to the identification and presentation of phenotype information on pathogenicity and effector genes and their host interactions. Specific gene alterations that did not alter the in host interaction phenotype are also presented. PHI-base is invaluable for comparative analyses and for the discovery of candidate targets in medically and agronomically important species for intervention. Version 4.12 (September 2021) contains 4387 references, and provides information on 8411 genes from 279 pathogens, tested on 228 hosts in 18, 190 interactions. This provides a 24% increase in gene content since Version 4.8 (September 2019). Bacterial and fungal pathogens represent the majority of the interaction data, with a 54:46 split of entries, whilst protists, protozoa, nematodes and insects represent 3.6% of entries. Host species consist of approximately 54% plants and 46% others of medical, veterinary and/or environmental importance. PHI-base data is disseminated to UniProtKB, FungiDB and Ensembl Genomes. PHI-base will migrate to a new gene-centric version (version 5.0) in early 2022. This major development is briefly described.
Assuntos
Bases de Dados Factuais , Interações Hospedeiro-Patógeno/genética , Fenótipo , Interface Usuário-Computador , Animais , Apicomplexa/classificação , Apicomplexa/genética , Apicomplexa/patogenicidade , Bactérias/classificação , Bactérias/genética , Bactérias/patogenicidade , Diplomonadida/classificação , Diplomonadida/genética , Diplomonadida/patogenicidade , Fungos/classificação , Fungos/genética , Fungos/patogenicidade , Insetos/classificação , Insetos/genética , Insetos/patogenicidade , Internet , Nematoides/classificação , Nematoides/genética , Nematoides/patogenicidade , Filogenia , Plantas/microbiologia , Plantas/parasitologia , VirulênciaRESUMO
Ensembl Genomes (https://www.ensemblgenomes.org) provides access to non-vertebrate genomes and analysis complementing vertebrate resources developed by the Ensembl project (https://www.ensembl.org). The two resources collectively present genome annotation through a consistent set of interfaces spanning the tree of life presenting genome sequence, annotation, variation, transcriptomic data and comparative analysis. Here, we present our largest increase in plant, metazoan and fungal genomes since the project's inception creating one of the world's most comprehensive genomic resources and describe our efforts to reduce genome redundancy in our Bacteria portal. We detail our new efforts in gene annotation, our emerging support for pangenome analysis, our efforts to accelerate data dissemination through the Ensembl Rapid Release resource and our new AlphaFold visualization. Finally, we present details of our future plans including updates on our integration with Ensembl, and how we plan to improve our support for the microbial research community. Software and data are made available without restriction via our website, online tools platform and programmatic interfaces (available under an Apache 2.0 license). Data updates are synchronised with Ensembl's release cycle.
Assuntos
Bases de Dados Genéticas , Genômica , Internet , Software , Animais , Biologia Computacional , Genoma Bacteriano/genética , Genoma Fúngico/genética , Genoma de Planta/genética , Plantas/classificação , Plantas/genética , Vertebrados/classificação , Vertebrados/genéticaRESUMO
The pathogen-host interactions database (PHI-base) is available at www.phi-base.org. PHI-base contains expertly curated molecular and biological information on genes proven to affect the outcome of pathogen-host interactions reported in peer reviewed research articles. PHI-base also curates literature describing specific gene alterations that did not affect the disease interaction phenotype, in order to provide complete datasets for comparative purposes. Viruses are not included, due to their extensive coverage in other databases. In this article, we describe the increased data content of PHI-base, plus new database features and further integration with complementary databases. The release of PHI-base version 4.8 (September 2019) contains 3454 manually curated references, and provides information on 6780 genes from 268 pathogens, tested on 210 hosts in 13,801 interactions. Prokaryotic and eukaryotic pathogens are represented in almost equal numbers. Host species consist of approximately 60% plants (split 50:50 between cereal and non-cereal plants), and 40% other species of medical and/or environmental importance. The information available on pathogen effectors has risen by more than a third, and the entries for pathogens that infect crop species of global importance has dramatically increased in this release. We also briefly describe the future direction of the PHI-base project, and some existing problems with the PHI-base curation process.
Assuntos
Doenças Transmissíveis/microbiologia , Doenças Transmissíveis/parasitologia , Biologia Computacional/métodos , Bases de Dados Factuais , Interações Hospedeiro-Patógeno/genética , Algoritmos , Animais , Antifúngicos , Bioensaio , Produtos Agrícolas , Gerenciamento de Dados , Genoma de Planta , Humanos , Internet , Fenótipo , Plantas , Ferramenta de BuscaRESUMO
In biology and biomedicine, relating phenotypic outcomes with genetic variation and environmental factors remains a challenge: patient phenotypes may not match known diseases, candidate variants may be in genes that haven't been characterized, research organisms may not recapitulate human or veterinary diseases, environmental factors affecting disease outcomes are unknown or undocumented, and many resources must be queried to find potentially significant phenotypic associations. The Monarch Initiative (https://monarchinitiative.org) integrates information on genes, variants, genotypes, phenotypes and diseases in a variety of species, and allows powerful ontology-based search. We develop many widely adopted ontologies that together enable sophisticated computational analysis, mechanistic discovery and diagnostics of Mendelian diseases. Our algorithms and tools are widely used to identify animal models of human disease through phenotypic similarity, for differential diagnostics and to facilitate translational research. Launched in 2015, Monarch has grown with regards to data (new organisms, more sources, better modeling); new API and standards; ontologies (new Mondo unified disease ontology, improvements to ontologies such as HPO and uPheno); user interface (a redesigned website); and community development. Monarch data, algorithms and tools are being used and extended by resources such as GA4GH and NCATS Translator, among others, to aid mechanistic discovery and diagnostics.
Assuntos
Biologia Computacional/métodos , Genótipo , Fenótipo , Algoritmos , Animais , Ontologias Biológicas , Bases de Dados Genéticas , Exoma , Estudos de Associação Genética , Variação Genética , Genômica , Humanos , Internet , Software , Pesquisa Translacional Biomédica , Interface Usuário-ComputadorRESUMO
Ensembl Genomes (http://www.ensemblgenomes.org) is an integrating resource for genome-scale data from non-vertebrate species, complementing the resources for vertebrate genomics developed in the context of the Ensembl project (http://www.ensembl.org). Together, the two resources provide a consistent set of interfaces to genomic data across the tree of life, including reference genome sequence, gene models, transcriptional data, genetic variation and comparative analysis. Data may be accessed via our website, online tools platform and programmatic interfaces, with updates made four times per year (in synchrony with Ensembl). Here, we provide an overview of Ensembl Genomes, with a focus on recent developments. These include the continued growth, more robust and reproducible sets of orthologues and paralogues, and enriched views of gene expression and gene function in plants. Finally, we report on our continued deeper integration with the Ensembl project, which forms a key part of our future strategy for dealing with the increasing quantity of available genome-scale data across the tree of life.
Assuntos
Biologia Computacional/métodos , Bases de Dados Genéticas , Variação Genética , Genoma Bacteriano , Genoma Fúngico , Genoma de Planta , Algoritmos , Animais , Caenorhabditis elegans/genética , Genômica , Internet , Anotação de Sequência Molecular , Fenótipo , Plantas/genética , Valores de Referência , Software , Interface Usuário-ComputadorRESUMO
The NLR-receptor RPP7 mediates race-specific immunity in Arabidopsis. Previous screens for enhanced downy mildew (edm) mutants identified the co-chaperone SGT1b (EDM1) and the PHD-finger protein EDM2 as critical regulators of RPP7. Here, we describe a third edm mutant compromised in RPP7 immunity, edm3. EDM3 encodes a nuclear-localized protein featuring an RNA-recognition motif. Like EDM2, EDM3 promotes histone H3 lysine 9 dimethylation (H3K9me2) at RPP7. Global profiling of H3K9me2 showed EDM3 to affect this silencing mark at a large set of loci. Importantly, both EDM3 and EDM2 co-associate in vivo with H3K9me2-marked chromatin and transcripts at a critical proximal polyadenylation site of RPP7, where they suppress proximal transcript polyadeylation/termination. Our results highlight the complexity of plant NLR gene regulation, and establish a functional and physical link between a histone mark and NLR-transcript processing.
Assuntos
Proteínas de Arabidopsis/metabolismo , Arabidopsis/metabolismo , Arabidopsis/genética , Proteínas de Arabidopsis/genética , Regulação da Expressão Gênica de Plantas/genética , Regulação da Expressão Gênica de Plantas/fisiologia , Proteínas de Ligação a RNA/genética , Proteínas de Ligação a RNA/metabolismoRESUMO
The pathogen-host interactions database (PHI-base) is available at www.phi-base.org PHI-base contains expertly curated molecular and biological information on genes proven to affect the outcome of pathogen-host interactions reported in peer reviewed research articles. In addition, literature that indicates specific gene alterations that did not affect the disease interaction phenotype are curated to provide complete datasets for comparative purposes. Viruses are not included. Here we describe a revised PHI-base Version 4 data platform with improved search, filtering and extended data display functions. A PHIB-BLAST search function is provided and a link to PHI-Canto, a tool for authors to directly curate their own published data into PHI-base. The new release of PHI-base Version 4.2 (October 2016) has an increased data content containing information from 2219 manually curated references. The data provide information on 4460 genes from 264 pathogens tested on 176 hosts in 8046 interactions. Prokaryotic and eukaryotic pathogens are represented in almost equal numbers. Host species belong â¼70% to plants and 30% to other species of medical and/or environmental importance. Additional data types included into PHI-base 4 are the direct targets of pathogen effector proteins in experimental and natural host organisms. The curation problems encountered and the future directions of the PHI-base project are briefly discussed.
Assuntos
Biologia Computacional/métodos , Bases de Dados Genéticas , Genômica/métodos , Interações Hospedeiro-Patógeno/genética , Curadoria de Dados , Fenótipo , Ferramenta de Busca , Interface Usuário-Computador , NavegadorRESUMO
PhytoPath (www.phytopathdb.org) is a resource for genomic and phenotypic data from plant pathogen species, that integrates phenotypic data for genes from PHI-base, an expertly curated catalog of genes with experimentally verified pathogenicity, with the Ensembl tools for data visualization and analysis. The resource is focused on fungi, protists (oomycetes) and bacterial plant pathogens that have genomes that have been sequenced and annotated. Genes with associated PHI-base data can be easily identified across all plant pathogen species using a BioMart-based query tool and visualized in their genomic context on the Ensembl genome browser. The PhytoPath resource contains data for 135 genomic sequences from 87 plant pathogen species, and 1364 genes curated for their role in pathogenicity and as targets for chemical intervention. Support for community annotation of gene models is provided using the WebApollo online gene editor, and we are working with interested communities to improve reference annotation for selected species.
Assuntos
Bases de Dados Genéticas , Genômica , Interações Hospedeiro-Patógeno/genética , Doenças das Plantas/microbiologia , Genes Bacterianos , Genes Fúngicos , Genoma Bacteriano , Genoma Fúngico , Oomicetos/genética , Fenótipo , Alinhamento de SequênciaRESUMO
The quantity and complexity of data being generated and published in biology has increased substantially, but few methods exist for capturing knowledge about phenotypes derived from molecular interactions between diverse groups of species, in such a way that is amenable to data-driven biology and research. To improve access to this knowledge, we have constructed a framework for the curation of the scientific literature studying interspecies interactions, using data curated for the Pathogen-Host Interactions database (PHI-base) as a case study. The framework provides a curation tool, phenotype ontology, and controlled vocabularies to curate pathogen-host interaction data, at the level of the host, pathogen, strain, gene, and genotype. The concept of a multispecies genotype, the 'metagenotype,' is introduced to facilitate capturing changes in the disease-causing abilities of pathogens, and host resistance or susceptibility, observed by gene alterations. We report on this framework and describe PHI-Canto, a community curation tool for use by publication authors.
The increasingly vast amount of data being produced in research communities can be difficult to manage, making it challenging for both humans and computers to organise and connect information from different sources. Currently, software tools that allow authors to curate peer-reviewed life science publications are designed solely for single species, or closely related species that do not interact. Although most research communities are striving to make their data FAIR (Findable, Accessible, Interoperable and Reusable), it is particularly difficult to curate detailed information based on interactions between two or more species (interspecies), such as pathogen-host interactions. As a result, there was a lack of tools to support multi-species interaction databases, leading to a reliance on labour-intensive curation methods. To address this problem, Cuzick et al. used the Pathogen-Host Interactions database (PHI-base), which curates knowledge from the text, tables and figures published in over 200 journals, as a case study. A framework was developed that could capture the many observable traits (phenotype annotations) for interactions and link them directly to the combination of genotypes involved in those interactions across multiple scales ranging from microscopic to macroscopic. This demonstrated that it was possible to build a framework of software tools to enable curation of interactions between species in more detail than had been done before. Cuzick et al. developed an online tool called PHI-Canto that allows any researcher to curate published pathogen-host interactions between almost any known species. An ontology a collection of concepts and their relations was created to describe the outcomes of pathogen-host interactions in a standardised way. Additionally, a new concept called the 'metagenotype' was developed which represents the combination of a pathogen and a host genotype and can be easily annotated with the phenotypes arising from each interaction. The newly curated multi-species FAIR data on pathogen-host interactions will enable researchers in different disciplines to compare and contrast interactions across species and scales. Ultimately, this will assist the development of new approaches to reduce the impact of pathogens on humans, livestock, crops and ecosystems with the aim of decreasing disease while increasing food security and biodiversity. The framework is potentially adoptable by any research community investigating interactions between species and could be adapted to explore other harmful and beneficial interspecies interactions.
Assuntos
Curadoria de Dados , Bases de Dados Factuais , Genótipo , FenótipoRESUMO
Fusarium culmorum causes ear blight disease on cereal crops resulting in considerable losses to grain yield, quality and safety. This fungus can also infect Arabidopsis floral tissues. In this study, the Arabidopsis floral infection model was used to assess the impact of five defence mutants on disease.Fusarium culmorum was spray inoculated onto the floral tissues of the mutantseds1, lms1, rar1, sgt1a and sgt1b involved in basal and resistance gene-mediated defence to pathogens. Floral disease development was assessed quantitatively.Only the sgt1b mutant exhibited a significantly different interaction phenotype compared with wild-type plants. The buds and flowers were more resistant to infection and developed milder symptoms, but had wild-type levels of deoxynivalenol (DON)mycotoxin. Microscopic studies indicated that to cause disease, F. culmorum requires plant cells in the invaded tissues to be competent to activate both a cell death response and a sustained oxidative burst. The sgt1a mutant exhibited a weak trend towards greater disease resistance in the new silique tissues. This study highlights that the SGT1-mediated signalling cascade(s), which had previously only been demonstrated to be required for Arabidopsis resistance against biotrophic pathogens, is causally involved in F. culmorum disease symptom development.
Assuntos
Proteínas de Arabidopsis/fisiologia , Arabidopsis/microbiologia , Proteínas de Ciclo Celular/fisiologia , Fusarium/fisiologia , Transdução de Sinais , Arabidopsis/genética , Arabidopsis/metabolismo , Proteínas de Arabidopsis/genética , Proteínas de Arabidopsis/metabolismo , Proteínas de Ciclo Celular/genética , Proteínas de Ciclo Celular/metabolismo , Flores/genética , Flores/metabolismo , Flores/microbiologia , Imunidade Inata/genética , Mutação , RNA Mensageiro/metabolismo , Espécies Reativas de Oxigênio/metabolismoRESUMO
New pathogen-host interaction mechanisms can be revealed by integrating mutant phenotype data with genetic information. PHI-base is a multi-species manually curated database combining peer-reviewed published phenotype data from plant and animal pathogens and gene/protein information in a single database.
RESUMO
The Ascomycete pathogen Fusarium graminearum can infect all cereal species and lower grain yield, quality and safety. The fungus can also cause disease on Arabidopsis thaliana. In this study, the disease-causing ability of two F. graminearum mutants was analysed to further explore the parallels between the wheat (Triticum aestivum) and Arabidopsis floral pathosystems. Wild-type F. graminearum (strain PH-1) and two isogenic transformants lacking either the mitogen-activated protein kinase MAP1 gene or the trichodiene synthase TRI5 gene were individually spray- or point-inoculated onto Arabidopsis and wheat floral tissue. Disease development was quantitatively assessed both macroscopically and microscopically and deoxynivalenol (DON) mycotoxin concentrations determined by enzyme-linked immunosorbent assay (ELISA). Wild-type strain inoculations caused high levels of disease in both plant species and significant DON production. The map1 mutant caused minimal disease and DON accumulation in both hosts. The tri5 mutant, which is unable to produce DON, exhibited reduced pathogenicity on wheat ears, causing only discrete eye-shaped lesions on spikelets which failed to infect the rachis. By contrast, the tri5 mutant retained full pathogenicity on Arabidopsis floral tissue. This study reveals that DON mycotoxin production is not required for F. graminearum to colonize Arabidopsis floral tissue.
Assuntos
Arabidopsis/microbiologia , Flores/microbiologia , Proteínas Fúngicas/genética , Proteínas Fúngicas/metabolismo , Fusarium/genética , Triticum/microbiologia , Fusarium/metabolismo , Fusarium/patogenicidade , Deleção de Genes , Regulação Fúngica da Expressão Gênica , VirulênciaRESUMO
The cereal ear blight fungal pathogen Fusarium culmorum can infect Arabidopsis floral tissue, causing disease symptoms and mycotoxin production. Here we assessed the effect of seven mutants and one transgenic overexpression line, residing in either the salicylic acid (SA), jasmonic acid (JA) or ethylene (ET) defence signalling pathways, on the outcome of the Fusarium-Arabidopsis floral interaction. The bacterial susceptiblity mutant eds11 was also assessed. Flowering plants were spray inoculated with F. culmorum conidia to determine the host responses to initial infection and subsequent colonization. Enhanced susceptibility and higher concentrations of deoxynivalenol mycotoxin were observed in buds and flowers of the npr1 and eds11 mutants than in the wild-type Col-0 plants. An effect of the other two defence signalling pathways on disease was either absent (ET/JA combined), absent/minimal (ET) or inconclusive (JA). Overall, this study highlights a role for NPR1 and EDS11 in basal defence against F. culmorum in some floral organs. This is the first time that any of these well-characterized defence signalling mutations have been evaluated for a role in floral defence in any plant species.
Assuntos
Proteínas de Arabidopsis/genética , Arabidopsis/genética , Arabidopsis/microbiologia , Fusarium/fisiologia , Proteínas de Arabidopsis/fisiologia , Flores/genética , Flores/microbiologia , Regulação da Expressão Gênica de Plantas , Interações Hospedeiro-Patógeno , Imunidade Inata/genética , Meristema/genética , Meristema/microbiologia , Doenças das Plantas/genética , Doenças das Plantas/microbiologia , Plantas Geneticamente Modificadas/genética , Plantas Geneticamente Modificadas/microbiologia , Transdução de Sinais/genética , Transdução de Sinais/fisiologiaRESUMO
Specific disease resistance of Arabidopsis thaliana against the Hyaloperonospora parasitica isolate Hiks1 (HpHiks1) is mediated by RPP7. Although this disease resistance gene encodes a typical nucleotide binding site leucine-rich repeat (NB-LRR) disease resistance protein, its function is independent of the defense hormone salicylic acid and most known genes required for plant immune responses. We identified EDM2 (enhanced downy mildew 2) in a genetic screen for RPP7 suppressors. Mutations of EDM2 phenocopy RPP7 mutations, but do not affect other tested disease resistance genes. We isolated EDM2 by map-based cloning. The predicted EDM2 protein is structurally unrelated to previously identified components of the plant immune system, bears typical features of transcriptional regulators, including plant homeodomain (PHD)-finger-like domains, and defines a plant-specific protein family. In edm2 mutants both constitutive and HpHiks1-induced RPP7 transcript levels are reduced, suggesting that EDM2 is either a direct or an indirect regulator of RPP7 expression. Microarray analyses defined a set of defense-associated genes, the expression of which is suppressed during successful HpHiks1 colonization of either rpp7 or edm2 plants. This transcriptional phenotype is counteracted by an EDM2/RPP7-dependent mechanism.
Assuntos
Proteínas de Arabidopsis/metabolismo , Arabidopsis/parasitologia , Regulação da Expressão Gênica de Plantas , Peronospora/fisiologia , Fatores de Transcrição/metabolismo , Sequência de Aminoácidos , Arabidopsis/genética , Arabidopsis/fisiologia , Cromossomos de Plantas , Genes de Plantas , Proteínas de Homeodomínio , Imunidade Inata , Dados de Sequência Molecular , Família Multigênica , Mutação , Análise de Sequência com Séries de Oligonucleotídeos , Doenças das Plantas/imunologia , Alinhamento de Sequência , Transdução de Sinais , Transcrição GênicaRESUMO
Type III secretion is a widespread method whereby Gram-negative bacteria introduce toxins into eukaryotic cells. These toxins mimic or subvert a normal cellular process by interacting with a specific target, although how toxins reach their site of action is unclear. We set out to investigate the intracellular localization of a type III toxin of Pseudomonas aeruginosa called ExoU, which has phospholipase activity and requires a eukaryotic factor for activity. We found that ExoU is localized to the plasma membrane and undergoes modification within the cell by addition of two ubiquitin molecules at lysine-178. A region of five amino acids at position 679-683 near the C-terminus of the ExoU protein controls both membrane localization and ubiquitinylation. Site-directed mutagenesis identified a tryptophan at position 681 as crucial for these effects. We found that the same region at position 679-683 was also required for cell toxicity produced by ExoU as well as in vitro phospholipase activity. Localization of the phospholipase ExoU to the plasma membrane is thus required for activation and allows efficient utilization of adjacent substrate phospholipids.
Assuntos
Proteínas de Bactérias/metabolismo , Toxinas Bacterianas/metabolismo , Pseudomonas aeruginosa/patogenicidade , Proteínas de Bactérias/química , Proteínas de Bactérias/genética , Proteínas de Bactérias/toxicidade , Toxinas Bacterianas/química , Toxinas Bacterianas/genética , Toxinas Bacterianas/toxicidade , Sequência de Bases , Membrana Celular/metabolismo , Membrana Celular/microbiologia , DNA Bacteriano/genética , Células HeLa , Humanos , Lisina/química , Modelos Biológicos , Peso Molecular , Mutagênese Sítio-Dirigida , Pseudomonas aeruginosa/genética , Proteínas Recombinantes/química , Proteínas Recombinantes/genética , Proteínas Recombinantes/metabolismo , Proteínas Recombinantes/toxicidade , Transfecção , Ubiquitina/química , Ubiquitina/metabolismoRESUMO
Microbial interactions with host cell signaling pathways are key determinants of the host cell response to infection. Many toxins secreted by bacterial type III secretion systems either stimulate or inhibit the host inflammatory response. We investigated the role of type III secreted toxins of the lung pathogen Pseudomonas aeruginosa in the inflammatory response of human respiratory epithelial cells to infection. Using bacteria with specific gene deletions, we found that interleukin-8 production by these cells was almost entirely dependent on bacterial type III secretion of exotoxin U (ExoU), a phospholipase, although other bacterial factors are involved. ExoU activated the c-Jun NH(2)-terminal kinase pathway, stimulating the phosphorylation and activation of mitogen-activated kinase kinase 4, c-Jun NH(2)-terminal kinase, and c-Jun. This in turn increased levels of transcriptionally competent activator protein-1. Although this pathway was dependent on the lipase activity of ExoU, it was independent of cell death. Activation of mitogen-activated kinase signaling by ExoU in this fashion is a novel mechanism by which a bacterial product can initiate a host inflammatory response, and it may result in increased epithelial permeability and bacterial spread.
Assuntos
Células Epiteliais/metabolismo , Exotoxinas/fisiologia , Interleucina-8/biossíntese , Proteínas Quinases JNK Ativadas por Mitógeno/fisiologia , Sistema de Sinalização das MAP Quinases/imunologia , Pseudomonas aeruginosa/fisiologia , Regulação para Cima , Células Epiteliais/enzimologia , Células Epiteliais/imunologia , Humanos , Pseudomonas aeruginosa/genética , Pseudomonas aeruginosa/patogenicidade , Regulação para Cima/imunologiaRESUMO
AvrRpt2, a Pseudomonas syringae type III effector protein, functions from inside plant cells to promote the virulence of P. syringae pv. tomato strain DC3000 (PstDC3000) on Arabidopsis thaliana plants lacking a functional copy of the corresponding RPS2 resistance gene. In this study, we extended our understanding of AvrRpt2 virulence activity by exploring the hypothesis that AvrRpt2 promotes PstDC3000 virulence by suppressing plant defenses. When delivered by PstDC3000, AvrRpt2 suppresses pathogen-related (PR) gene expression during infection, suggesting that AvrRpt2 suppresses defenses mediated by salicylic acid (SA). However, AvrRpt2 promotes PstDC3000 growth on transgenic plants expressing the SA-degrading enzyme NahG, indicating that AvrRpt2 does not promote bacterial virulence by modulating SA levels during infection. AvrRpt2 general virulence activity does not depend on the RPM1 resistance gene, as mutations in RPM1 had no effect on AvrRpt2-induced phenotypes. Transgenic plants expressing AvrRpt2 displayed enhanced susceptibility to PstDC3000 strains defective in type III secretion, indicating that enhanced susceptibility of these plants is not because of suppression of defense responses elicited by other type III effectors. Additionally, avrRpt2 transgenic plants did not exhibit increased susceptibility to Peronospora parasitica and Erysiphe cichoracearum, suggesting that AvrRpt2 virulence activity is specific to P. syringae.
Assuntos
Arabidopsis/genética , Proteínas de Bactérias/genética , Pseudomonas syringae/patogenicidade , Ácido Salicílico/metabolismo , Arabidopsis/metabolismo , Arabidopsis/microbiologia , Proteínas de Arabidopsis/genética , Proteínas de Arabidopsis/metabolismo , Proteínas de Bactérias/metabolismo , Fungos/crescimento & desenvolvimento , Regulação Bacteriana da Expressão Gênica , Regulação da Expressão Gênica de Plantas , Imunidade Inata/genética , Oxigenases de Função Mista/genética , Oxigenases de Função Mista/metabolismo , Mutação , Peronospora/crescimento & desenvolvimento , Doenças das Plantas/microbiologia , Proteínas de Plantas/genética , Proteínas de Plantas/metabolismo , Plantas Geneticamente Modificadas , Transdução de Sinais/genética , Virulência/genéticaRESUMO
We describe the identification of a mutant in the Arabidopsis accession Columbia (Col-0) that exhibits enhanced downy mildew (edm1) susceptibility to several Peronospora parasitica isolates, including the RPP7-diagnostic isolate Hiks1. The mutation was mapped to chromosome IV and characterized physically as a 35-kb deletion spanning seven genes. One of these genes complemented the mutant to full wild-type resistance against all of the Peronospora isolates tested. This gene (AtSGT1b) encodes a predicted protein of 39.8 kD and is an Arabidopsis ortholog of yeast SGT1, which was described originally as a key regulatory protein in centromere function and ubiquitin-mediated proteolysis. AtSGT1b contains three tetratricopeptide repeats at the N terminus followed by a bipartite chord-containing SGT domain and an SGT-specific domain at the C terminus. We discuss the role of AtSGT1b in disease resistance and its possible involvement in ubiquitin-mediated proteolysis in plants.