The plant genes required for the growth and reproduction of plant pathogens are largely unknown. In an effort to identify these genes, we isolated Arabidopsis mutants that do not support the normal growth of the powdery mildew pathogen Erysiphe cichoracearum . Here, we report on the cloning and characterization of one of these genes, PMR6 . PMR6 encodes a pectate lyase-like protein with a novel C-terminal domain. Consistent with its predicted gene function, mutations in PMR6 alter the composition of the plant cell wall, as shown by Fourier transform infrared spectroscopy. pmr6 -mediated resistance requires neither salicylic acid nor the ability to perceive jasmonic acid or ethylene, indicating that the resistance mechanism does not require the activation of well-described defense pathways. Thus, pmr6 resistance represents a novel form of disease resistance based on the loss of a gene required during a compatible interaction rather than the activation of known host defense pathways.

BackgroundThe hypersensitive necrosis response (HR) of resistant plants to avirulent pathogens is a form of programmed cell death in which the plant sacrifices a few cells under attack, restricting pathogen growth into adjacent healthy tissues. In spite of the importance of this defense response, relatively little is known about the plant components that execute the cell death program or about its regulation in response to pathogen attack.ResultsWe isolated the edr2-6 mutant, an allele of the previously described edr2 mutants. We found that edr2-6 exhibited an exaggerated chlorosis and necrosis response to attack by three pathogens, two powdery mildew and one downy mildew species, but not in response to abiotic stresses or attack by the bacterial leaf speck pathogen. The chlorosis and necrosis did not spread beyond inoculated sites suggesting that EDR2 limits the initiation of cell death rather than its spread. The pathogen-induced chlorosis and necrosis of edr2-6 was correlated with a stimulation of the salicylic acid defense pathway and was suppressed in mutants deficient in salicylic acid signaling. EDR2 encodes a novel protein with a pleckstrin homology and a StAR transfer (START) domain as well as a plant-specific domain of unknown function, DUF1336. The pleckstrin homology domain binds to phosphatidylinositol-4-phosphate in vitro and an EDR2:HA:GFP protein localizes to endoplasmic reticulum, plasma membrane and endosomes.ConclusionEDR2 acts as a negative regulator of cell death, specifically the cell death elicited by pathogen attack and mediated by the salicylic acid defense pathway. Phosphatidylinositol-4-phosphate may have a role in limiting cell death via its effect on EDR2. This role in cell death may be indirect, by helping to target EDR2 to the appropriate membrane, or it may play a more direct role.

To further the understanding of the natural genetic diversity for disease resistance to powdery mildew (Erysiphe cichoracearum) in Arabidopsis thaliana, quantitative trait loci analysis was undertaken on recombinant inbred lines derived from a cross between the resistant accession Warschau-1 and the susceptible Columbia-0. Powdery mildew grew less well on Warschau-1, but the resistance was not associated with a specific block in the infection sequence. Two potential powdery mildew disease-resistance loci were identified and mapped, one with a major effect and one with a minor effect on disease resistance. The two loci acted in an additive manner to confer resistance, and together they explained 65% of the variation in resistance. In addition, the major powdery mildew disease-resistance locus was genetically mapped to the bottom of chromosome III, a region containing the powdery mildew resistance loci RPW7, RPW8 and RPW10. Unlike resistance mediated by the RPW8 locus in the accession Moscow-1, resistance in Warschau-1 was not correlated with the hypersensitive response, highlighting the influence of genetic background or environmental factors on the expression of disease resistance. Together with the powdery mildew resistance loci described in other studies, these results suggest that A. thaliana is a useful source of natural powdery mildew disease resistance, which potentially can be utilized in fundamental studies and as a tool for applied studies.

Powdery mildew diseases are economically important diseases, caused by obligate biotrophic fungi of the Erysiphales. To understand the complex inheritance of resistance to the powdery mildew disease in the model plant Arabidopsis thaliana, quantitative trait loci analysis was performed using a set of recombinant inbred lines derived from a cross between the resistant accession Kashmir-1 and the susceptible accession Columbia glabrous1. We identified and mapped three independent powdery mildew quantitative disease resistance loci, which act additively to confer disease resistance. The locus with the strongest effect on resistance was mapped to a 500-kbp interval on chromosome III.

No abstract