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BAH1/NLA是一种环状泛素E3连接酶,可调节水杨酸的积累以及对丁香假单胞菌DC3000的免疫反应。

BAH1/NLA, a RING-type ubiquitin E3 ligase, regulates the accumulation of salicylic acid and immune responses to Pseudomonas syringae DC3000.

作者信息

Yaeno Takashi, Iba Koh

机构信息

Department of Biology, Faculty of Sciences, Kyushu University, Hakozaki, Fukuoka, Japan.

出版信息

Plant Physiol. 2008 Oct;148(2):1032-41. doi: 10.1104/pp.108.124529. Epub 2008 Aug 27.

DOI:10.1104/pp.108.124529
PMID:18753285
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2556844/
Abstract

Salicylic acid (SA) is a primary factor responsible for exerting diverse immune responses in plants and is synthesized in response to attack by a wide range of pathogens. The Arabidopsis (Arabidopsis thaliana) sid2 mutant is defective in a SA biosynthetic pathway involving ISOCHORISMATE SYNTHASE1 (ICS1) and consequently contains reduced levels of SA. However, the sid2 mutant as well as ICS-suppressed tobacco (Nicotiana benthamiana) still accumulate a small but significant level of SA. These observations along with previous studies suggest that SA might also be synthesized by another pathway involving benzoic acid (BA). Here we isolated a benzoic acid hypersensitive1-Dominant (bah1-D) mutant that excessively accumulated SA after application of BA from activation-tagged lines. This mutant also accumulated higher levels of SA after inoculation with Pseudomonas syringae pv tomato DC3000. Analysis of the bah1-D sid2 double mutant suggested that the bah1-D mutation caused both ICS1-dependent and -independent accumulation. In addition, the bah1-D mutant showed SA-dependent localized cell death in response to P. syringae pv tomato DC3000. The T-DNA insertional mutation that caused the bah1-D phenotypes resulted in the suppression of expression of the NLA gene, which encodes a RING-type ubiquitin E3 ligase. These results suggest that BAH1/NLA plays crucial roles in the ubiquitination-mediated regulation of immune responses, including BA- and pathogen-induced SA accumulation, and control of cell death.

摘要

水杨酸(SA)是植物中引发多种免疫反应的主要因素,它在植物受到多种病原体攻击时被合成。拟南芥(Arabidopsis thaliana)的sid2突变体在涉及异分支酸合酶1(ICS1)的SA生物合成途径中存在缺陷,因此SA水平降低。然而,sid2突变体以及ICS被抑制的烟草(Nicotiana benthamiana)仍会积累少量但显著水平的SA。这些观察结果以及先前的研究表明,SA也可能通过另一条涉及苯甲酸(BA)的途径合成。在这里,我们从激活标签系中分离出一个苯甲酸超敏1显性(bah1-D)突变体,该突变体在施用BA后会过度积累SA。该突变体在接种丁香假单胞菌番茄致病变种DC3000后也积累了更高水平的SA。对bah1-D sid2双突变体的分析表明,bah1-D突变导致了ICS1依赖性和非依赖性积累。此外,bah1-D突变体在响应丁香假单胞菌番茄致病变种DC3000时表现出SA依赖性的局部细胞死亡。导致bah1-D表型的T-DNA插入突变导致了编码RING型泛素E3连接酶的NLA基因表达受到抑制。这些结果表明,BAH1/NLA在泛素化介导的免疫反应调节中起关键作用,包括BA和病原体诱导的SA积累以及细胞死亡的控制。