Bacterial effectors target the common signaling partner BAK1 to disrupt multiple MAMP receptor-signaling complexes and impede plant immunity

被引:433
作者
Shan, Libo [1 ]
He, Ping [1 ]
Li, Jianming [2 ]
Heese, Antje [3 ]
Peck, Scott C. [3 ]
Nuernberger, Thorsten [4 ]
Martin, Gregory B. [5 ,6 ]
Sheen, Jen [1 ]
机构
[1] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA
[2] Univ Michigan, Dept Mol Cellular & Dev Biol, Ann Arbor, MI 48109 USA
[3] Univ Missouri, Dept Biochem, Columbia, MO 65211 USA
[4] Univ Tubingen, ZMBP, D-72076 Tubingen, Germany
[5] Cornell Univ, Boyce Thompson Inst Plant Res, Ithaca, NY 14853 USA
[6] Cornell Univ, Dept Plant Pathol & Plant Microbe Biol, Ithaca, NY 14853 USA
关键词
D O I
10.1016/j.chom.2008.05.017
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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.
引用
收藏
页码:17 / 27
页数:11
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