Signal transduction in the plant immune response

McDowell, John M.; Dangl, Jeffery L.

doi:10.1016/s0968-0004(99)01532-7

Cited by 450 publications

(281 citation statements)

References 26 publications

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“…One possibility for what this factor might be is nitric oxide. It is also possible that both ROS and nitric oxide (and perhaps other signals) contribute to the plant cell's decision to undergo programmed cell death (McDowell and Dangl, 2000).…”

Section: Discussionmentioning

confidence: 99%

The Role ofNDR1in Avirulence Gene-Directed Signaling and Control of Programmed Cell Death in Arabidopsis

2001

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Arabidopsis plants containing the ndr1-1 mutation are incapable of mounting a hypersensitive response to bacteria carrying avrRpt2, but show an exaggerated cell death response to bacteria carrying avrB (Century et al., 1995). We show here that ndr1-1 plants are severely impaired in induction of systemic acquired resistance and PR1-driven transcription of a reporter gene in response to Pseudomonas syringae strains carrying avrRpt2 but not in response to P. syringae carrying avrB. The ndr1-1 mutation also impaired salicylic acid (SA) accumulation in response to treatments that produced reactive oxygen species (ROS) and impaired induction of systemic acquired resistance in response to in situ production of ROS. Hydrogen peroxide accumulated in wild-type Arabidopsis leaves beginning 4 to 7 h postinoculation with P. syringae carrying either avrRpt2 or avrB. In ndr1-1 plants, P. syringae carrying avrRpt2 elicited no detectable hydrogen peroxide production. Hydrogen peroxide production in response to bacteria carrying avrB was similar to that of Columbia in kinetics but of lesser intensity at early time points. These data are interpreted to indicate that NDR1 links ROS generation to SA production and that the phenotypic consequences of the ndr1-1 mutation are caused by a reduced ability to accumulate SA upon pathogen infection.Exquisite specificity is a hallmark of gene-for-gene disease resistance. Individual plant lines carry a specific complement of disease resistance (R) genes. Plants resist infection only if the pathogen carries a specific avirulence (avr) gene that is the matched cognate of one of these plant R genes. Mutant plants with nonfunctional alleles of a particular R gene fail to recognize a pathogen carrying the corresponding avr gene, and disease ensues (Parker et al., 2000;Staskawicz, 2001). With bacterial pathogens, this specificity of molecular recognition in at least some cases is associated with direct binding of the plant R gene product to the bacterial avr gene product (Scofield et al., 1996; Tang et al., 1996). Recognition takes place inside the plant cell (Gopalan et al., 1996;Leister et al., 1996) following export of the avr gene product from the bacteria via a type III secretion system (Pirhonen et al., 1996;Mudgett and Staskawicz, 1998).In contrast to the specificity of upstream molecular recognition processes, downstream plant responses to pathogen infection often bear strong similarities despite being elicited by vastly different types of pathogen. Gene-for-gene disease resistance is usually accompanied by rapid cell death (the hypersensitive response [HR]; Klement, 1982) in plant cells that are in direct contact with pathogen (Turner and Novacky, 1974). Uninoculated regions of the plant are induced to display an immunity to further pathogen challenge termed systemic acquired resistance (SAR). SAR protects plants from a broad spectrum of pathogens including those very different from the original (Ryals et al., 1994). A set of genes termed "pathogenesis related" (PR) are induced both locall...

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Section: Discussionmentioning

confidence: 99%

The Role ofNDR1in Avirulence Gene-Directed Signaling and Control of Programmed Cell Death in Arabidopsis

2001

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“…One such response involves recognition of pathogen-encoded ligands by plant disease resistance ( R ) gene products (Gabriel and Rolfe, 1990). This recognition event initiates signaling pathways that lead to hypersensitive response (localized cell death) at the site of pathogen ingress, rapid oxidative burst, cell wall strengthening, protein phosphorylation, and activation of various defense response genes (McDowell and Dangl, 2000). These events are followed by a nonspecific general defense response throughout the plant called systemic acquired resistance (Ryals et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Role of SCF Ubiquitin-Ligase and the COP9 Signalosome in the N Gene–Mediated Resistance Response to Tobacco mosaic virus

et al. 2002

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“…Some of the inducible defenses have been shown to depend on the concerted action of two phytohormones, ethylene and jasmonate (Feys and Parker, 2000;McDowell and Dangl, 2000;Glazebrook, 2001;Thomma et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

ETHYLENE RESPONSE FACTOR1 Integrates Signals from Ethylene and Jasmonate Pathways in Plant Defense[W]

et al. 2003

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Cross-talk between ethylene and jasmonate signaling pathways determines the activation of a set of defense responses against pathogens and herbivores. However, the molecular mechanisms that underlie this cross-talk are poorly understood. Here, we show that ethylene and jasmonate pathways converge in the transcriptional activation of ETHYLENE RESPONSE FACTOR1 (ERF1), which encodes a transcription factor that regulates the expression of pathogen response genes that prevent disease progression. The expression of ERF1 can be activated rapidly by ethylene or jasmonate and can be activated synergistically by both hormones. In addition, both signaling pathways are required simultaneously to activate ERF1 , because mutations that block any of them prevent ERF1 induction by any of these hormones either alone or in combination. Furthermore, 35S : ERF1 expression can rescue the defense response defects of coi1 ( coronative insensitive1 ) and ein2 ( ethylene insensitive2 ); therefore, it is a likely downstream component of both ethylene and jasmonate signaling pathways. Transcriptome analysis in Col; 35S : ERF1 transgenic plants and ethylene/ jasmonate-treated wild-type plants further supports the notion that ERF1 regulates in vivo the expression of a large number of genes responsive to both ethylene and jasmonate. These results suggest that ERF1 acts downstream of the intersection between ethylene and jasmonate pathways and suggest that this transcription factor is a key element in the integration of both signals for the regulation of defense response genes.

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Signal transduction in the plant immune response

Cited by 450 publications

References 26 publications

The Role ofNDR1in Avirulence Gene-Directed Signaling and Control of Programmed Cell Death in Arabidopsis

The Role ofNDR1in Avirulence Gene-Directed Signaling and Control of Programmed Cell Death in Arabidopsis

Role of SCF Ubiquitin-Ligase and the COP9 Signalosome in the N Gene–Mediated Resistance Response to Tobacco mosaic virus

ETHYLENE RESPONSE FACTOR1 Integrates Signals from Ethylene and Jasmonate Pathways in Plant Defense[W]

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