Proteomics and Functional Analyses of Pepper Abscisic Acid-Responsive 1 (ABR1), Which Is Involved in Cell Death and Defense Signaling

Proteomics and Functional Analyses of Pepper Abscisic Acid-Responsive 1 (ABR1), Which Is Involved in Cell Death and Defense Signaling
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DOI:
10.1105/tpc.110.082081
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发表时间:
2011-02-01
期刊:
影响因子:
11.6
通讯作者:
Hwang, Byung Kook
Hwang, Byung Kook
中科院分区:
生物学1区
文献类型:
--
作者:
Choi, Du Seok;Hwang, Byung Kook

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脱落酸(阿坝)是植物生长发育和防御反应的重要调节因子。高通量植物蛋白质组筛选鉴定了辣椒(辣椒)中含有ABA-应答1(ABR 1)结构域的葡萄糖基转移酶、Rab-like GT3激活剂和肌管蛋白,ABR 1通过无毒野油菜黄单胞菌vesicatoria感染和阿坝处理高度诱导。ABR 1结构域对于细胞死亡反应和ABR 1的核定位是必需的。ABR 1是引发细胞死亡和活性氧产生以及ABA-水杨酸(SA)拮抗作用所必需的。ABR 1的沉默显着削弱了过敏反应,但提高了辣椒中细菌病原体的生长和阿坝水平。在ABR 1沉默的植物中,高水平的阿坝拮抗病原菌感染诱导的SA水平。ABR 1在拟南芥中的异源转基因表达增强了对番茄假单胞菌和透明霜霉的抗性。拟南芥ABR 1假定的直系同源突变体,abr 1,对这些病原体的易感性也支持ABR 1参与抗病性。总之,这些结果揭示了ABR 1作为阿坝信号传导的一种新的负调节因子,并表明核ABR 1库对于与ABA-SA拮抗作用相关的细胞死亡诱导是必不可少的。
Abscisic acid (ABA) is a key regulator of plant growth and development, as well as plant defense responses. A high-throughput in planta proteome screen identified the pepper (Capsicum annuum) GRAM (for glucosyltransferases, Rab-like GTPase activators, and myotubularins) domain-containing ABA-RESPONSIVE1 (ABR1), which is highly induced by infection with avirulent Xanthomonas campestris pv vesicatoria and also by treatment with ABA. The GRAM domain is essential for the cell death response and for the nuclear localization of ABR1. ABR1 is required for priming cell death and reactive oxygen species production, as well as ABA-salicylic acid (SA) antagonism. Silencing of ABR1 significantly compromised the hypersensitive response but enhanced bacterial pathogen growth and ABA levels in pepper. High levels of ABA in ABR1-silenced plants antagonized the SA levels induced by pathogen infection. Heterologous transgenic expression of ABR1 in Arabidopsis thaliana conferred enhanced resistance to Pseudomonas syringae pv tomato and Hyaloperonospora arabidopsidis infection. The susceptibility of the Arabidopsis ABR1 putative ortholog mutant, abr1, to these pathogens also supports the involvement of ABR1 in disease resistance. Together, these results reveal ABR1 as a novel negative regulator of ABA signaling and suggest that the nuclear ABR1 pool is essential for the cell death induction associated with ABA-SA antagonism.