Yaeno Takashi, Iba Koh
Department of Biology, Faculty of Sciences, Kyushu University, Hakozaki, Fukuoka, Japan.
Plant Physiol. 2008 Oct;148(2):1032-41. doi: 10.1104/pp.108.124529. Epub 2008 Aug 27.
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.
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。