Pathogen Effectors Target Arabidopsis EDS1 and Alter Its Interactions with Immune Regulators

被引：239

作者：

Bhattacharjee, Saikat ^{[1
,2
]}

Halane, Morgan K. ^{[3
]}

Kim, Sang Hee ^{[1
,2
]}

Gassmann, Walter ^{[1
,2
]}

机构：

[1] Univ Missouri, Christopher S Bond Life Sci Ctr, Div Plant Sci, Columbia, MO 65211 USA

[2] Univ Missouri, Interdisciplinary Plant Grp, Columbia, MO 65211 USA

[3] Univ Missouri, Dept English, Columbia, MO 65211 USA

来源：

SCIENCE | 2011年 / 334卷 / 6061期

基金：

美国国家科学基金会;

关键词：

DISEASE RESISTANCE; INNATE IMMUNITY; PLANT IMMUNITY; REPEAT PROTEIN; RECEPTORS; SYSTEM; GENES; SRFR1;

D O I：

10.1126/science.1211592

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Plant resistance proteins detect the presence of specific pathogen effectors and initiate effector-triggered immunity. Few immune regulators downstream of resistance proteins have been identified, none of which are known virulence targets of effectors. We show that Arabidopsis ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1), a positive regulator of basal resistance and of effector-triggered immunity specifically mediated by Toll-interleukin-1 receptor-nucleotide binding-leucine-rich repeat (TIR-NB-LRR) resistance proteins, forms protein complexes with the TIR-NB-LRR disease resistance proteins RPS4 and RPS6 and with the negative immune regulator SRFR1 at a cytoplasmic membrane. Further, the cognate bacterial effectors AvrRps4 and HopA1 disrupt these EDS1 complexes. Tight association of EDS1 with TIR-NB-LRR-mediated immunity may therefore derive mainly from being guarded by TIR-NB-LRR proteins, and activation of this branch of effector-triggered immunity may directly connect to the basal resistance signaling pathway via EDS1.

引用

页码：1405 / 1408

页数：4

共 28 条

[1] Different requirements for EDS1 and NDR1 by disease resistance genes define at least two R gene-mediated signaling pathways in Arabidopsis [J].