|Debroy, Sruti - MICHIGAN STATE U|
|Kwack, Yong-Bum - MICHIGAN STATE U|
|Nomura, Kinya - MICHIGAN STATE U|
|He, Sheng Yang - MICHIGAN STATE U|
Submitted to: Proceedings of the National Academy of Sciences
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 12, 2004
Publication Date: June 29, 2004
Citation: Debroy, S., Thilmony, R.L., Kwack, Y., Nomura, K., He, S. 2004. A famliy of conserved bacterial effectors inhibits salicylic acid-meditated basal immunity and promotes disease necrosis in plants. Proceedings of the National Academy of Sciences. 101: 9927-9932 Interpretive Summary: Plant disease causes significant crop losses annually. Our understanding of how plant pathogens cause disease is limited. The goal of this research is to increase our understanding of the molecular mechanisms underlying plant susceptibility to bacterial infection. This research characterized how several bacterial virulence proteins contribute to the ability of the pathogen to cause disease on its host plant. These bacterial proteins suppress host plant resistance promoting pathogen growth and disease symptom development.
Technical Abstract: Salicylic acid (SA)-mediated host immunity plays a central role in combating microbial pathogens in plants. It was shown that mutations in conserved effector loci (CEL) in the plant pathogens Pseudomonas syringae (the DCEL mutation), Erwinia amylovora (the dspA/E mutation), and Pantoea stewartii subsp. stewartii (the wtsE mutation) exert particularly strong negative effects on bacterial virulence in their host plants via unknown mechanisms. We found that the loss of virulence in DCEL and dspA/E mutants was linked to their inability to suppress cell wall-based defenses and to cause normal disease necrosis in Arabidopsis and apple host plants. The DCEL mutant activated SA-dependent callose deposition in wild-type Arabidopsis, but failed to elicit high levels of callose-associated defense in Arabidopsis plants blocked in SA accumulation or synthesis. This mutant also multiplied more aggressively in SA-deficient plants than in wild-type plants. The hopPtoM and avrE genes in the CEL of P. syringae were found to encode suppressors of this SA-dependent basal defense. The widespread conservation of the HopPtoM and AvrE families of effectors in various bacteria suggests that suppression of SA-dependent basal immunity is an important virulence strategy for successful infection of plants by diverse necrosis-causing bacteria.