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PAMP-triggered immunity components and LysM-receptor-like kinases.

机译:PAMP触发的免疫成分和LysM受体样激酶。

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摘要

In order to identify components of Pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) pathways in Nicotiana benthamiana , a large-scale forward-genetics screen using virus-induced gene silencing and a cell-death-based assay for assessing PTI was performed. The assay relied on four combinations of PTI-inducing non-pathogens and cell-death-causing challenger pathogens, and was first validated in plants silenced for FLS2 or BAK1. Over 3,200 genes were screened and 14 genes were identified that, when silenced, compromised PTI. A subset of the genes was found to act downstream of FLS2-mediated PTI induction and silencing of three genes compromised production of reactive oxygen species (ROS) in leaves exposed to flg22. The 14 genes encode proteins with potential functions in defense and hormone signaling, protein stability and degradation, energy and secondary metabolism and cell wall biosynthesis and provide a new resource to explore the molecular basis for the involvement of these processes in PTI.;Peptidoglycan (PGN) has been shown to trigger immune responses in Arabidopsis thaliana. However, in tomato, PGN did not trigger archetypal immune responses such as mitogen-activated protein kinase activation, ROS production or protection from subsequent bacterial infections. This lack of responses suggests that PGN is not involved in activating immunity and stopping bacterial colonization in tomato. In A. thaliana, immunity against bacteria requires LysM-receptor-like kinases (LysM-RLKs). Two tomato LysM-RLKs, SlBti9 and SlLyk13, were shown to be required for resistance against both pathogenic and non-pathogenic Pseudomonas syringae pv. tomato. Flagellin-mediated responses were compromised in plants silenced for SlBti9 and SlLyk13, which could explain the increased bacterial susceptibility observed in these plants. RNAi of SlBti9 and SlLyk13 also compromised chitin perception, as was reported previously for A. thaliana LysM-RLK CERK1. Auto-phosphorylation seems to be required for the activity of these two tomato LysM-RLKs in immunity as cell death mediated by over-expression of these proteins in N. benthamiana was abolished in kinase-inactive mutants. SlBti9 and/or SlLyk13 probably function as either pattern recognition receptors for a yet uncharacterized bacterial PAMP or are part of the receptor complex to transduce the signal once the recognition event has occurred.
机译:为了确定本生烟草中病原相关分子模式(PAMP)触发的免疫(PTI)途径的组成部分,使用病毒诱导的基因沉默和基于细胞死亡的评估PTI的大规模前向遗传学筛选被执行了。该测定法依赖于诱导PTI的非病原体和引起细胞死亡的攻击者病原体的四种组合,并且首先在沉默了FLS2或BAK1的植物中进行了验证。筛选了3200多个基因,鉴定出14个基因,这些基因沉默后会破坏PTI。发现该基因的一个子集在FLS2介导的PTI诱导下游起作用,而三个基因的沉默则会降低暴露于flg22的叶片中活性氧(ROS)的产生。这14个基因编码在防御和激素信号传导,蛋白质稳定性和降解,能量和次级代谢以及细胞壁生物合成中具有潜在功能的蛋白质,并为探索这些过程参与PTI的分子基础提供了新的资源。 )已显示出可以在拟南芥中触发免疫反应。但是,在番茄中,PGN不会触发原型免疫反应,如促分裂原活化的蛋白激酶活化,ROS产生或免受随后的细菌感染。这种缺乏应答表明PGN不参与激活免疫力和停止番茄中的细菌定植。在拟南芥中,对细菌的免疫需要LysM受体样激酶(LysM-RLKs)。两个番茄LysM-RLKs,SlBti9和SlLyk13,被证明对致病性和非致病性丁香假单胞菌PV都有抗性。番茄。在针对SlBti9和SlLyk13沉默的植物中鞭毛蛋白介导的反应受到损害,这可以解释在这些植物中观察到的细菌敏感性增加。如先前关于拟南芥LysM-RLK CERK1的报道,SlBti9和SlLyk13的RNAi也损害了几丁质的感知。这两个番茄LysM-RLK在免疫中的活性似乎需要自磷酸化,因为在激酶失活的突变体中消除了由本氏烟草中这些蛋白的过表达介导的细胞死亡。 S1Bti9和/或S1Lyk13可能充当尚未表征的细菌PAMP的模式识别受体,或者是一旦发生识别事件就转导信号的受体复合物的一部分。

著录项

  • 作者单位

    Cornell University.;

  • 授予单位 Cornell University.;
  • 学科 Botany.
  • 学位 Ph.D.
  • 年度 2012
  • 页码 228 p.
  • 总页数 228
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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