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首页> 外文期刊>Plant physiology >BAH1/NLA, a RING-type ubiquitin E3 ligase, regulates the accumulation of salicylic acid and immune responses to Pseudomonas syringae DC3000
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BAH1/NLA, a RING-type ubiquitin E3 ligase, regulates the accumulation of salicylic acid and immune responses to Pseudomonas syringae DC3000

机译:BAH1 / NLA,一种RING型泛素E3连接酶,调节水杨酸的积累和对丁香假单胞菌DC3000的免疫应答

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摘要

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.
机译:水杨酸(SA)是负责在植物中发挥多种免疫反应的主要因子,是响应多种病原体侵袭而合成的。拟南芥(Arabidopsis thaliana)sid2突变体在涉及ISOCHORISMATE SYNTHASE1(ICS1)的SA生物合成途径中存在缺陷,因此其SA水平降低。但是,sid2突变体以及ICS抑制的烟草(Nicotiana benthamiana)仍然积累了少量但显着水平的SA。这些观察结果以及以前的研究表明,SA可能还通过另一种涉及苯甲酸(BA)的途径合成。在这里,我们从激活标记品系中分离出BA后应用过量的SA积累了一个苯甲酸超敏1显性(bah1-D)突变体。接种丁香假单胞菌PV番茄DC3000后,该突变体还积累了较高水平的SA。对bah1-D sid2双重突变体的分析表明bah1-D突变引起了ICS1依赖性和非依赖性累积。此外,bah1-D突变体显示出对丁香假单胞菌pv番茄DC3000的SA依赖性局部细胞死亡。导致bah1-D表型的T-DNA插入突变导致NLA基因表达的抑制,该基因编码RING型泛素E3连接酶。这些结果表明,BAH1 / NLA在泛素介导的免疫反应调节中起着关键作用,包括BA和病原体诱导的SA积累,以及对细胞死亡的控制。

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