| Autor: |
Yulei Shang, Xinyan Li, Haitao Cui, Ping He, Thilmony, Roger, Chintamanani, Satya, Zwiesler-Vollick, Julie, Gopalan, Suresh, Tang, Xiaoyan, Zhou, Jian-Min |
| Předmět: |
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| Zdroj: |
Proceedings of the National Academy of Sciences of the United States of America; 12/12/2006, Vol. 103 Issue 50, p19200-19205, 6p |
| Abstrakt: |
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 Pseudo- monas syringae effector AvrB suppresses PAMP-triggered immunity (P11) through RAR1, a cochaperone of HSP9O required for ETI. AvrB expressed in plants lacking the cognate resistance gene RPM1 sup- presses cell wall defense induced by the flagellar peptide flg22, a well known PAMP, and promotes the growth of nonpathogenic bacteria in a R4RI-dependent manner. ran 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 Fri. effector virulence, and ETI. The study supports that both pathogen virulence and plant disease resistance have evolved around P11. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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