<i>NDR1</i>
            , a Pathogen-Induced Component Required for
            <i>Arabidopsis</i>
            Disease Resistance

Century, Karen S.; Shapiro, Allan D.; Repetti, Peter P.; Dahlbeck, Douglas; Holub, Eric B.; Staskawicz, Brian J.

doi:10.1126/science.278.5345.1963

Cited by 346 publications

(253 citation statements)

References 20 publications

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“…It should be possible to gain further insights into the roles of CNGC4 and CNGC2 within the complex interplay of plant defense signaling networks by examination of the mutant phenotypes in response to other pathogens whose specificities are mediated by the EDS1 signaling pathway (Aarts et al, 1998), by exploration of the roles of SGT1, RAR1, and NPR1, other downstream signaling components, and through expression analysis of a much wider array of genes. The rapid induction of the transcription of HLM1 by ethylene/jasmonate and by Xanthomonas, similar to that observed for PAD4 (Jirage et al, 1999), EDS1 (Falk et al, 1999), NDR1 (Century et al, 1997), and EDS5 (Nawrath et al, 2002) in response to pathogens, would favor such an approach.…”

Section: Discussionmentioning

confidence: 99%

HLM1, an Essential Signaling Component in the Hypersensitive Response, Is a Member of the Cyclic Nucleotide–Gated Channel Ion Channel Family[W]

et al. 2003

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The hypersensitive response (HR) in plants is a programmed cell death that is commonly associated with disease resistance. A novel mutation in Arabidopsis, hlm1 , which causes aberrant regulation of cell death, manifested by a lesionmimic phenotype and an altered HR, segregated as a single recessive allele. Broad-spectrum defense mechanisms remained functional or were constitutive in the mutant plants, which also exhibited increased resistance to a virulent strain of Pseudomonas syringae pv tomato . In response to avirulent strains of the same pathogen, the hlm1 mutant showed differential abilities to restrict bacterial growth, depending on the avirulence gene expressed by the pathogen. The HLM1 gene encodes a cyclic nucleotide-gated channel, CNGC4 . Preliminary study of the HLM1/CNGC4 gene product in Xenopus oocytes (inside-out patch-clamp technique) showed that CNGC4 is permeable to both K ؉ and Na ؉ and is activated by both cGMP and cAMP. HLM1 gene expression is induced in response to pathogen infection and some pathogen-related signals. Thus, HLM1 might constitute a common downstream component of the signaling pathways leading to HR/resistance.

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Section: Discussionmentioning

confidence: 99%

HLM1, an Essential Signaling Component in the Hypersensitive Response, Is a Member of the Cyclic Nucleotide–Gated Channel Ion Channel Family[W]

et al. 2003

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“…Tests of epistasis were performed by crossing resistant Pi-0 sober1-1 plants with the following mutants: Col-0 ndr1-1 (Century et al, 1997), Ler eds1-2 (Falk et al, 1999), Col-0 pad4-1 (Jirage et al, 1999), Col-0 jar1-1 (Staswick et al, 2002), Col-0 sid2-1 (Dewdney et al, 2000;Wildermuth et al, 2001), and Col-0 npr1-1 (Cao et al, 1997). In planta growth curves were determined with F3 families established from independent F2 double mutant individuals to quantify the growth of Pst DC3000 AvrBsT Hyb -HA.…”

Section: Genetic Components Of Avrbst-elicited Disease Resistancementioning

confidence: 99%

A Conserved Carboxylesterase Is a SUPPRESSOR OF AVRBST-ELICITED RESISTANCE inArabidopsis

et al. 2007

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AvrBsT is a type III effector from Xanthomonas campestris pv vesicatoria that is translocated into plant cells during infection. AvrBsT is predicted to encode a Cys protease that targets intracellular host proteins. To dissect AvrBsT function and recognition in Arabidopsis thaliana, 71 ecotypes were screened to identify lines that elicit an AvrBsT-dependent hypersensitive response (HR) after Xanthomonas campestris pv campestris (Xcc) infection. The HR was observed only in the Pi-0 ecotype infected with Xcc strain 8004 expressing AvrBsT. To create a robust pathosystem to study AvrBsT immunity in Arabidopsis, the foliar pathogen Pseudomonas syringae pv tomato (Pst) strain DC3000 was engineered to translocate AvrBsT into Arabidopsis by the Pseudomonas type III secretion (T3S) system. Pi-0 leaves infected with Pst DC3000 expressing a Pst T3S signal fused to AvrBsT-HA (AvrBsT HYB -HA) elicited HR and limited pathogen growth, confirming that the HR leads to defense. Resistance in Pi-0 is caused by a recessive mutation predicted to inactivate a carboxylesterase known to hydrolyze lysophospholipids and acylated proteins in eukaryotes. Transgenic Pi-0 plants expressing the wild-type Columbia allele are susceptible to Pst DC3000 AvrBsT HYB -HA infection. Furthermore, wild-type recombinant protein cleaves synthetic p-nitrophenyl ester substrates in vitro. These data indicate that the carboxylesterase inhibits AvrBsT-triggered phenotypes in Arabidopsis. Here, we present the cloning and characterization of the SUPPRESSOR OF AVRBST-ELICITED RESISTANCE1.

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“…NDR1 was first identified in a genetic screen aimed at identifying genetic loci required for disease resistance signaling in Arabidopsis in response to infection by P. syringae (Century et al, 1995(Century et al, , 1997. NDR1 is a plasma membrane, glycophosphatidyl-inositol (GPI)-anchored protein required for the activation of disease resistance signaling mediated by members of the largest class of disease resistance proteins in Arabidopsis (Coppinger et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

NDR1 Interaction with RIN4 Mediates the Differential Activation of Multiple Disease Resistance Pathways in Arabidopsis

2006

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Recognition of pathogens by plants involves the coordinated efforts of molecular chaperones, disease resistance (R) proteins, and components of disease resistance signaling pathways. Characterization of events associated with pathogen perception in Arabidopsis thaliana has advanced understanding of molecular genetic mechanisms associated with disease resistance and protein interactions critical for the activation of resistance signaling. Regulation of R protein-mediated signaling in response to the bacterial pathogen Pseudomonas syringae in Arabidopsis involves the physical association of at least two R proteins with the negative regulator RPM1 INTERACTING PROTEIN4 (RIN4). While the RIN4-RPS2 (for RESISTANCE TO P. SYRINGAE2) and RIN4-RPM1 (for RESISTANCE TO P. SYRINGAE PV MACULICOLA1) signaling pathways exhibit differential mechanisms of activation in terms of effector action, the requirement for NON-RACE-SPECIFIC DISEASE RESISTANCE1 (NDR1) is shared. Using a yeast two-hybrid screen, followed by a series of coimmunoprecipitation experiments, we demonstrate that the RIN4-NDR1 interaction occurs on the cytoplasmically localized N-terminal portion of NDR1 and that this interaction is required for the activation of resistance signaling following infection by P. syringae expressing the Cys protease Type III effector protein AvrRpt2. We demonstrate that like RPS2 and RPM1, NDR1 also associates with RIN4 in planta. We suggest that this interaction serves to further regulate activation of disease resistance signaling following recognition of P. syringae DC3000-AvrRpt2 by Arabidopsis.

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NDR1 , a Pathogen-Induced Component Required for Arabidopsis Disease Resistance

Cited by 346 publications

References 20 publications

HLM1, an Essential Signaling Component in the Hypersensitive Response, Is a Member of the Cyclic Nucleotide–Gated Channel Ion Channel Family[W]

HLM1, an Essential Signaling Component in the Hypersensitive Response, Is a Member of the Cyclic Nucleotide–Gated Channel Ion Channel Family[W]

A Conserved Carboxylesterase Is a SUPPRESSOR OF AVRBST-ELICITED RESISTANCE inArabidopsis

NDR1 Interaction with RIN4 Mediates the Differential Activation of Multiple Disease Resistance Pathways in Arabidopsis

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