Submitted to: Proceedings of the National Academy of Sciences
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/24/2006
Publication Date: 12/5/2006
Citation: Shang, Y., Li, X., Cui, H., He, P., Thilmony, R.L., Chintamanani, S., Zwiesler-Vollick, J., Gopalan, S., Tang, X., Zhou, J. 2006. Rar1, a central player in plant immunity, is targeted by pseudomonas syringae effector avrb. Proceedings of the National Academy of Sciences. PNAS vol. 103 no. 50 pg. 19200-19205
Interpretive Summary: Plant disease causes significant crop losses and our understanding of how plant pathogens cause disease is limited. This research demonstrates how a protein from a bacterial pathogen weakens the ability of the host plant to defend itself from disease. In particular the relationship between this pathogen protein and a plant protein required for resistance is investigated. This research demonstrates that a plant protein involved in pathogen resistance is also a target for a bacterial protein that impairs host defenses and promotes the ability of the pathogen to cause disease.
Technical Abstract: Pathogenic bacterial effectors suppress Pathogen-Associated Molecular Pattern (PAMP)-triggered host immunity, thereby promoting parasitism. In the presence of cognate resistance genes, it is proposed that plants detect the virulence activity of bacterial effectors and trigger a defense response, referred to here as effector-triggered immunity. However, the link between effector virulence and effector-triggered immunity at the molecular level is unknown. Here, we show that the Pseudomonas syringae effector AvrB suppresses PAMP-triggered immunity through RAR1, a co-chaperone of HSP90 required for effector-triggered immunity. AvrB expressed in plants lacking the cognate resistance gene RPM1 suppresses cell wall defense induced by the flagellar peptide flg22, a well-known PAMP, and promotes the growth of nonpathogenic bacteria in a RAR1-dependent manner. rar1 mutants display enhanced cell wall defense in response to flg22, indicating that RAR1 negatively regulates PAMP-triggered immunity. Furthermore, coimmunoprecipitation experiments indicated that RAR1 and AvrB interact in the plant. The results demonstrate that RAR1 molecularly links PAMP-triggered immunity, the effector virulence, and effector-triggered immunity. The study supports that both pathogen virulence and plant disease resistance have evolved around the PAMP-triggered immunity.