RAR1, a central player in plant immunity, is targeted by Pseudomonas syringae effector AvrB
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, ref...
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Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 103; no. 50; pp. 19200 - 19205 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
National Academy of Sciences
12.12.2006
National Acad Sciences |
Subjects | |
Online Access | Get full text |
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Summary: | 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 (ETI). However, the link between effector virulence and ETI at the molecular level is unknown. Here, we show that the Pseudomonas syringae effector AvrB suppresses PAMP-triggered immunity (PTI) through RAR1, a cochaperone of HSP90 required for ETI. 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 PTI. Furthermore, coimmunoprecipitation experiments indicated that RAR1 and AvrB interact in the plant. The results demonstrate that RAR1 molecularly links PTI, effector virulence, and ETI. The study supports that both pathogen virulence and plant disease resistance have evolved around PTI. |
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Bibliography: | http://dx.doi.org/10.1073/pnas.0607279103 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Edited by Brian J. Staskawicz, University of California, Berkeley, CA, and approved October 24, 2006 Author contributions: Y.S., X.L., and H.C. contributed equally to this work; X.L. and J.-M.Z. designed research; Y.S., X.L., H.C., P.H., R.T., and S.C. performed research; R.T., J.Z.-V., S.G., and J.-M.Z. contributed new reagents/analytic tools; Y.S., X.L., X.T., and J.-M.Z. analyzed data; and X.T. and J.-M.Z. wrote the paper. |
ISSN: | 0027-8424 1091-6490 |
DOI: | 10.1073/pnas.0607279103 |