Jeff Dangl

The Dangl lab is interested in how plants recognize and fend off pathogens. The lab employs all the modern tools of genetics, genomics and biochemistry to identify the molecular players in this recognition system, and to figure out how plants ward off attack by bacterial and fungal pathogens. The lab uses the model plant species Arabidopsis thaliana to identify all the plant genes necessary for a resistance reaction against the phytopathogenic bacterium Pseudomonas syringae and an oomycete parasite called Peronospora parasitica. Their work revolves around three main themes:

(1) Understanding the structure and function of plant NB-LRR disease resistance proteins.
The Arabidopsis genome encodes about 125 genes for the NB-LRR plant immune system, which is named for the two domains of the specific recognition element these genes contain. Each NB-LRR protein conditions resistance to a particular strain of pathogen. The Dangl lab was among the first to demonstrate that NB-LRR proteins probably work by monitoring or detecting the action of pathogen virulence factors as they attempt to alter the host cell. They are currently using genetics and biochemistry to understand how this process is controlled.

(2) The control of programmed cell death that accompanies R-gene action.
The earliest events following R-gene (resistance reaction gene) engagement are ion fluxes at the plasma membrane and the generation of superoxide and nitric oxide. Calcium influx and phosphorylation cascades have also been implicated as defense responses. All of these events lead to a massive transcriptional re-programming and, in many cases, to a very rapid cell death at the site of attempted infection. The Dangl lab is interested in identifying the genes responsible for these events to gain insight into pathogen-mediated programmed cell death in plants.

(3) Understanding the molecular mechanism by which pathogenic bacteria cause disease in plants.
A high-throughput FACS-based genomics approach is being taken by the Dangl lab to identify all of the virulence factors or “type III effector genes” carried in each of 16 strains of Pseudomonas syringae. In addition, host targets of these factors and previously identified factors are also being cloned and analyzed. Genetic and biochemical characterization of virulence factors and their host targets will shed light on the mechanism of bacterial pathogenesis in plants.

Selected Publications:
Fahlgren N, Howell MD, Kasschau KD, Chapman EJ, Sullivan CM, Cumbie JS, Givan SA, Law TF, Grant SR, Dangl JL, Carrington JC. (2007) High-Throughput Sequencing of Arabidopsis microRNAs: Evidence for Frequent Birth and Death of MIRNA Genes. PLoS ONE. 2:e219.

Kaminaka H, Nake C, Epple P, Dittgen J, Schutze K, Chaban C, Holt BF 3rd, Merkle T, Schafer E, Harter K, Dangl JL. (2006) bZIP10-LSD1 antagonism modulates basal defense and cell death in Arabidopsis following infection. EMBO J. 25:4400-11.

Dangl JL, McDowell JM. (2006) Two modes of pathogen recognition by plants. Proc Natl Acad Sci U S A. 103:8575-6.

Torres MA, Jones JD, Dangl JL. (2005) Pathogen-induced, NADPH oxidase-derived reactive oxygen intermediates suppress spread of cell death in Arabidopsis thaliana. Nat Genet 37:1130-4.

Holt BF 3rd, Belkhadir Y, Dangl JL. (2005) Antagonistic control of disease resistance protein stability in the plant immune system. Science 309:929-32.

Belkhadir Y, Nimchuk Z, Hubert DA, Mackey D and Dangl JL (2004) Arabidopsis RIN4 negatively regulates disease resistance mediated by RPS2 and RPM1 downstream or independent of the NDR1 signal modulator, and is not required for the virulence functions of bacterial type III effectors AvrRpt2 or AvrRpm1. Plant Cell 16:2822-2835.







				The Dangl lab is interested in how plants recognize and fend off pathogens. The lab employs all the modern tools of genetics, genomics and biochemistry to identify the molecular players in this recognition system, and to figure out how plants ward off attack by bacterial and fungal pathogens. The lab uses the model plant species Arabidopsis thaliana to identify all the plant genes necessary for a resistance reaction against the phytopathogenic bacterium Pseudomonas syringae and an oomycete parasite called Peronospora parasitica. Their work revolves around three main themes: (1) Understanding the structure and function of plant NB-LRR disease resistance proteins. The Arabidopsis genome encodes about 125 genes for the NB-LRR plant immune system, which is named for the two domains of the specific recognition element these genes contain. Each NB-LRR protein conditions resistance to a particular strain of pathogen. The Dangl lab was among the first to demonstrate that NB-LRR proteins probably work by monitoring or detecting the action of pathogen virulence factors as they attempt to alter the host cell. They are currently using genetics and biochemistry to understand how this process is controlled. (2) The control of programmed cell death that accompanies R-gene action. The earliest events following R-gene (resistance reaction gene) engagement are ion fluxes at the plasma membrane and the generation of superoxide and nitric oxide. Calcium influx and phosphorylation cascades have also been implicated as defense responses. All of these events lead to a massive transcriptional re-programming and, in many cases, to a very rapid cell death at the site of attempted infection. The Dangl lab is interested in identifying the genes responsible for these events to gain insight into pathogen-mediated programmed cell death in plants. (3) Understanding the molecular mechanism by which pathogenic bacteria cause disease in plants. A high-throughput FACS-based genomics approach is being taken by the Dangl lab to identify all of the virulence factors or “type III effector genes” carried in each of 16 strains of Pseudomonas syringae. In addition, host targets of these factors and previously identified factors are also being cloned and analyzed. Genetic and biochemical characterization of virulence factors and their host targets will shed light on the mechanism of bacterial pathogenesis in plants. Selected Publications: Fahlgren N, Howell MD, Kasschau KD, Chapman EJ, Sullivan CM, Cumbie JS, Givan SA, Law TF, Grant SR, Dangl JL, Carrington JC. (2007) High-Throughput Sequencing of Arabidopsis microRNAs: Evidence for Frequent Birth and Death of MIRNA Genes. PLoS ONE. 2:e219. Kaminaka H, Nake C, Epple P, Dittgen J, Schutze K, Chaban C, Holt BF 3rd, Merkle T, Schafer E, Harter K, Dangl JL. (2006) bZIP10-LSD1 antagonism modulates basal defense and cell death in Arabidopsis following infection. EMBO J. 25:4400-11. Dangl JL, McDowell JM. (2006) Two modes of pathogen recognition by plants. Proc Natl Acad Sci U S A. 103:8575-6. Torres MA, Jones JD, Dangl JL. (2005) Pathogen-induced, NADPH oxidase-derived reactive oxygen intermediates suppress spread of cell death in Arabidopsis thaliana. Nat Genet 37:1130-4. Holt BF 3rd, Belkhadir Y, Dangl JL. (2005) Antagonistic control of disease resistance protein stability in the plant immune system. Science 309:929-32. Belkhadir Y, Nimchuk Z, Hubert DA, Mackey D and Dangl JL (2004) Arabidopsis RIN4 negatively regulates disease resistance mediated by RPS2 and RPM1 downstream or independent of the NDR1 signal modulator, and is not required for the virulence functions of bacterial type III effectors AvrRpt2 or AvrRpm1. Plant Cell 16:2822-2835.



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