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Jeff Dangl


John N. Couch Professor

Contact Information

Office: 4260 Genome Sciences Building
Email: dangl[at]email.unc.edu
Office Phone: (919) 962-4469
Lab Phone: (919) 537-3890

Dangl Lab Website

Research Description

At a Glance

  • How do plants recognize pathogens?
  • How do disease resistance mechanisms evolve?
  • Can we engineer “novel” disease resistance in crops?

Synopsis

Many interactions between plants and microbes begin with specific recognition. The nature of this recognition, and the interpretation of subsequent signal transduction by both plant and microbe have profound impact on the outcome of the interaction. Plants have evolved effective mechanisms to recognize pathogenic microbes and halt their biotrophic or necrotrophic growth in the plant. Active plant defense mechanisms obviously force the selection of microbe variants which can evade the plant’s recognition capabilities. This evolutionary tug of war has led to a complex set of both plant and microbe genes, whose interactions lead to a successful plant resistance reaction. As well as a potentially large array of cognitive gene functions, a number of subsequent signal transduction steps must be necessary to generate a completely effective resistant phenotype.

Genetic analyses in many systems over the last 50 years have demonstrated that recognition functions are provided by dominant alleles of genes in the plant (Resistance, or R-genes) which interact, either directly or indirectly, with either the direct or indirect product of a single pathogen gene (avirulence, or avr genes). This so called “gene-for-gene” hypothesis is a genetic explanation for interactions between plants and all classes of pathogens: fungal, bacterial, viral, and insect. In the last two years, eight new resistance genes were cloned from various species, and they share certain structural features.

Arabidopsis thaliana

We use a model plant species, Arabidopsis thaliana, to identify genetically the plant loci necessary for a resistance reaction against phytopathogenic bacteria and fungus. Our work revolves around four themes. First, isolation of recognition function genes (R or Resistance genes). We use mutation analysis to identify loci which give rise to either loss of recognition, or constitutive induction of a resistance-like phenotype. Second, we isolated mutants in processes involved in control of plant cell death. Third, we are cloning a cluster of R genes directed against a fungal pathogen with the express intent to understand evolution of both R protein function and the evolution of specificity. Fourth, we are identifying the bacterial pathogen genes which are causal to triggering of a specific plant defense response.

We have recently cloned and analyzed the RPM1 disease resistance gene from Arabidopsis. The RPM1 gene confers dual specificity to pathogens expressing either of two unrelated avr genes. Despite this novel function, RPM1 encodes a protein sharing molecular features with recently described single-specificity R genes. Surprisingly, this gene is lacking from naturally occurring susceptible Arabidopsis accessions. Our continuing goals are to analyze how these protein functions to enable disease resistance using both genetic and cell biological methods, and to understand its evolution both within Arabidopsis and its Brassica relatives.

Our second interest regards programmed cell death in plants. We initially isolated four Arabidopsis mutants which exhibit aberrant cell death control. These mutations define four loci (termed lsd1 and lsd3-lsd5 based on their Lesions Simulating Disease Resistance phenotype). They can be divided further into three loci controlling the initiation of cell death, and one which determines the propagation of cell death once it is initiated externally. These mutants also exhibit cell-type specificity for onset of cell death, implying that cell death initiation in Arabidopsis can be controlled by spatial and developmental cues. We are concentrating on two mutants with contrasting phenotypes: lsd1 which defines the “propagation class” of loci involved in limiting the spread of cell death; and lsd5, a mutant which uniquely triggers cell death specifically in leaf epidermal cells (the others initiate cell death in the leaf mesophyll). We have shown a critical role for superoxide radicals in the spread of cell death associated with the lsd1 mutant phenotype. We are near the end point in cloning of these two genes, and have isolated extragenic suppresser mutants for each.

The third project, isolation and analysis of a fungal disease resistance gene cluster from Arabidopsis, is in the beginning phase.

 

Our fourth interest is in bacterial genetics of the Pseudomonas syringae pathogens of Arabidopsis. We have isolated the avr gene, avrRpm1, which defines the RPM1 disease resistance gene, and have shown that this avr function is also required for maximal virulence on susceptible Arabidopsis plants which do not contain a functional RPM1 gene. We have also isolated a novel and interesting mutant which, although it is unable to deliver avrRpm1 or avrB-dependent signals to Arabidopsis, retains the ability to deliver the signal from a third gene, avrRpt2. This finding is interesting because it is the first bacterial mutation to date that separates signal delivery of various avr gene functions to resistant plants.

Cross-section of Bacterial infected leaf tissue.

 

For a recent magazine article on part of the Dangl Lab’s research see: http://research.unc.edu/endeavors/win98/dangltl.html

Articles about the Arabidopsis genome sequence:

From The New York Times