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本文引用的文献

1
The atypical resistance gene, RPW8, recruits components of basal defence for powdery mildew resistance in Arabidopsis.非典型抗性基因RPW8招募基础防御成分以实现拟南芥对白粉病的抗性。
Plant J. 2005 Apr;42(1):95-110. doi: 10.1111/j.1365-313X.2005.02356.x.
2
Mutations in PMR5 result in powdery mildew resistance and altered cell wall composition.PMR5基因的突变导致对白粉病的抗性以及细胞壁成分的改变。
Plant J. 2004 Dec;40(6):968-78. doi: 10.1111/j.1365-313X.2004.02264.x.
3
The mitochondrion--an organelle commonly involved in programmed cell death in Arabidopsis thaliana.线粒体——一种通常参与拟南芥程序性细胞死亡的细胞器。
Plant J. 2004 Nov;40(4):596-610. doi: 10.1111/j.1365-313X.2004.02239.x.
4
START lipid/sterol-binding domains are amplified in plants and are predominantly associated with homeodomain transcription factors.起始脂质/固醇结合结构域在植物中得到扩增,并且主要与同源异型域转录因子相关。
Genome Biol. 2004;5(6):R41. doi: 10.1186/gb-2004-5-6-r41. Epub 2004 May 27.
5
Oleic acid levels regulated by glycerolipid metabolism modulate defense gene expression in Arabidopsis.由甘油脂质代谢调节的油酸水平调控拟南芥中的防御基因表达。
Proc Natl Acad Sci U S A. 2004 Apr 6;101(14):5152-7. doi: 10.1073/pnas.0401315101. Epub 2004 Mar 25.
6
Genome-wide analysis of membrane targeting by S. cerevisiae pleckstrin homology domains.酿酒酵母普列克底物蛋白同源结构域膜靶向的全基因组分析。
Mol Cell. 2004 Mar 12;13(5):677-88. doi: 10.1016/s1097-2765(04)00083-8.
7
The Arabidopsis thaliana dihydroxyacetone phosphate reductase gene SUPPRESSSOR OF FATTY ACID DESATURASE DEFICIENCY1 is required for glycerolipid metabolism and for the activation of systemic acquired resistance.拟南芥磷酸二羟丙酮还原酶基因脂肪酸去饱和酶缺陷抑制因子1对于甘油脂代谢和系统获得性抗性的激活是必需的。
Plant Cell. 2004 Feb;16(2):465-77. doi: 10.1105/tpc.016907. Epub 2004 Jan 16.
8
Molecular machinery for non-vesicular trafficking of ceramide.神经酰胺非囊泡运输的分子机制
Nature. 2003 Dec 18;426(6968):803-9. doi: 10.1038/nature02188.
9
Ceramides modulate programmed cell death in plants.神经酰胺调节植物中的程序性细胞死亡。
Genes Dev. 2003 Nov 1;17(21):2636-41. doi: 10.1101/gad.1140503. Epub 2003 Oct 16.
10
Arabidopsis sfd mutants affect plastidic lipid composition and suppress dwarfing, cell death, and the enhanced disease resistance phenotypes resulting from the deficiency of a fatty acid desaturase.拟南芥sfd突变体影响质体脂质组成,并抑制因脂肪酸去饱和酶缺陷导致的矮化、细胞死亡和增强的抗病表型。
Plant Cell. 2003 Oct;15(10):2383-98. doi: 10.1105/tpc.015529. Epub 2003 Sep 24.

含PH和START结构域的蛋白EDR2对拟南芥植物防御反应的调控

Regulation of plant defense responses in Arabidopsis by EDR2, a PH and START domain-containing protein.

作者信息

Tang Dingzhong, Ade Jules, Frye Catherine A, Innes Roger W

机构信息

Department of Biology, Indiana University, Bloomington, IN 47405, USA.

出版信息

Plant J. 2005 Oct;44(2):245-57. doi: 10.1111/j.1365-313X.2005.02523.x.

DOI:10.1111/j.1365-313X.2005.02523.x
PMID:16212604
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1797612/
Abstract

We have identified an Arabidopsis mutant that displays enhanced disease resistance (edr2) to the biotrophic powdery mildew pathogen Erysiphe cichoracearum. Inhibition of fungal growth on edr2 mutant leaves occurred at a late stage of the infection process and coincided with formation of necrotic lesions approximately 5 days after inoculation. Double-mutant analysis revealed that edr2-mediated resistance is suppressed by mutations that inhibit salicylic acid (SA)-induced defense signaling, including npr1, pad4 and sid2, demonstrating that edr2-mediated disease resistance is dependent on SA. However, edr2 showed normal responses to the bacterial pathogen Pseudomonas syringae pv. tomato strain DC3000. EDR2 appears to be constitutively transcribed in all tissues and organs and encodes a novel protein, consisting of a putative pleckstrin homology (PH) domain and a steroidogenic acute regulatory protein-related lipid-transfer (START) domain, and contains an N-terminal mitochondrial targeting sequence. The PH and START domains are implicated in lipid binding, suggesting that EDR2 may provide a link between lipid signaling and activation of programmed cell death mediated by mitochondria.

摘要

我们鉴定出了一种拟南芥突变体,它对活体营养型白粉病病原体菊苣白粉菌表现出增强的抗病性(edr2)。在感染过程的后期,真菌在edr2突变体叶片上的生长受到抑制,且这与接种后约5天坏死病斑的形成同时发生。双突变分析表明,edr2介导的抗性被抑制水杨酸(SA)诱导防御信号传导的突变所抑制,这些突变包括npr1、pad4和sid2,这表明edr2介导的抗病性依赖于SA。然而,edr2对细菌病原体番茄丁香假单胞菌番茄致病变种DC3000表现出正常反应。EDR2似乎在所有组织和器官中组成型转录,编码一种新型蛋白质,该蛋白质由一个假定的普列克底物蛋白同源(PH)结构域和一个类固醇生成急性调节蛋白相关脂质转运(START)结构域组成,并含有一个N端线粒体靶向序列。PH和START结构域与脂质结合有关,这表明EDR2可能在脂质信号传导与线粒体介导的程序性细胞死亡激活之间建立联系。