BIOTECHNOLOGICAL ENHANCEMENT OF ENERGY CROPS
Location: Genomics and Gene Discovery
Title: EDR2 NEGATIVELY REGULATES SALICYLIC ACID-BASED DEFENSES AND CELL DEATH DURING POWDERY MILDEW INFECTIONS OF ARABIDOPSIS THALIANA
| Vorwerk, Sonja - CARNEGIE INSTITUTION |
| Schiff, Celine - CARNEGIE INSTITUTION |
| Santamaria, Marjorie - CARNEGIE INSTITUTION |
| Koh, Serry - CARNEGIE INSTITUTION |
| Nishimura, Marc - CARNEGIE INSTITUTION |
| Somerville, Chris - CARNEGIE INSTITUTION |
| Somerville, Shauna - CARNEGIE INSTITUTION |
Submitted to: Biomed Central (BMC) Plant Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 6, 2007
Publication Date: July 6, 2007
Citation: Vorwerk, S., Schiff, C., Santamaria, M., Koh, S., Nishimura, M., Vogel, J., Somerville, C., Somerville, S. 2007 EDR2 negatively regulates salicylic acid-based defenses and cell death during powdery mildew infections of Arabidopsis thaliana. BMC Plant Biology. 7: Issue 35 (on-line journal).
Interpretive Summary: To defend themselves against pathogen attack, plants often use a defense mechanism called the hypersensitive necrosis response in which a few cells at the site of pathogen infection are sacrificed in order to prevent the pathogen from spreading into adjacent healthy tissue. To gain a deeper understating of this response, the authors identified and characterized an Arabidopsis mutant, edr2-6, that exhibits an exaggerated necrosis when attacked by pathogens. It was shown that the edr2-6 phenotype was dependent upon signaling through the salicylic acid-dependent defense pathway. The corresponding gene was cloned and the possible significance of the protein domains discussed.
The 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. We isolated the edr2-6 mutant, which 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 ER, plasma membrane and endosomes. EDR2 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.