期刊
CELL HOST & MICROBE
卷 4, 期 1, 页码 17-27出版社
CELL PRESS
DOI: 10.1016/j.chom.2008.05.017
关键词
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资金
- NIGMS NIH HHS [R01 GM70567, R01 GM078021, R01 GM078021-01A1, R01 GM078021-04, R01GM078021, R01 GM078021-03, R01 GM078021-02, R01 GM070567] Funding Source: Medline
Successful pathogens have evolved strategies to interfere with host immune systems. For example, the ubiquitous plant pathogen Pseudomonas syringae injects two sequence-distinct effectors, AvrPto and AvrPtoB, to intercept convergent innate immune responses stimulated by multiple microbe-associated molecular patterns (MAMPs). However, the direct host targets and precise molecular mechanisms of bacterial effectors remain largely obscure. We show that AvrPto and AvrPtoB bind the Arabidopsis receptor-like kinase BAK1, a shared signaling partner of both the flagellin receptor FLS2 and the brassinosteroid receptor BRI1. This targeting interferes with ligand-dependent association of FLS2 with BAK1 during infection. It also impedes BAKI1 dependent host immune responses to diverse other MAMPs and brassinosteroid signaling. Significantly, the structural basis of AvrPto-BAK1 interaction appears to be distinct from AvrPto-Pto association required for effector-triggered immunity. These findings uncover a unique strategy of bacterial pathogenesis where virulence effectors block signal transmission through a key common component of multiple MAMP-receptor complexes.
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