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拟南芥中的内源性肽防御信号差异放大先天免疫反应的信号传导。

Endogenous peptide defense signals in Arabidopsis differentially amplify signaling for the innate immune response.

作者信息

Huffaker Alisa, Ryan Clarence A

机构信息

Institute of Biological Chemistry, Washington State University, Pullman, WA 99164-6340, USA.

出版信息

Proc Natl Acad Sci U S A. 2007 Jun 19;104(25):10732-6. doi: 10.1073/pnas.0703343104. Epub 2007 Jun 12.

Abstract

AtPep1, a 23-aa peptide encoded by Arabidopsis PROPEP1, a member of a small, six-member gene family, activates expression of the defense gene PDF1.2 (encoding defensin) and its own precursor gene, PROPEP1, through the jasmonate/ethylene signaling pathway, mediated by a cell-surface receptor, PEPR1. Overexpression of two family members, PROPEP1 and PROPEP2, enhances resistance of Arabidopsis plants against the pathogen Pythium irregulare, and PROPEP2 and PROPEP3 are expressed at highly elevated levels in Arabidopsis in response to pathogen infections and to several pathogen-associated molecules (general elicitors). Here, we report that PDF1.2, PR-1 (pathogenesis protein), and PROPEP genes were differentially expressed in the leaves of intact plants sprayed with methyl jasmonate and methyl salicylate and in excised leaves supplied through cut petioles with peptides derived from the C terminus of each of the encoded proteins. The expression of PDF1.2 and PR-1 elicited by the peptides was blocked in mutant plants deficient in the jasmonate/ethylene and salicylate pathways, and in wild-type plants by treatment with diphenylene iodonium chloride, an inhibitor of hydrogen peroxide production. PROPEP1, PROPEP 2, and PROPEP3 genes appear to have roles in a feedback loop that amplifies defense signaling pathways initiated by pathogens.

摘要

AtPep1是一种由拟南芥PROPEP1编码的23个氨基酸的肽,PROPEP1是一个由6个成员组成的小基因家族的成员,它通过细胞表面受体PEPR1介导的茉莉酸/乙烯信号通路,激活防御基因PDF1.2(编码防御素)及其自身前体基因PROPEP1的表达。两个家族成员PROPEP1和PROPEP2的过表达增强了拟南芥植物对病原体不规则腐霉的抗性,并且PROPEP2和PROPEP3在拟南芥中对病原体感染和几种病原体相关分子(通用激发子)的响应中表达水平大幅升高。在这里,我们报告PDF1.2、PR-1(病程相关蛋白)和PROPEP基因在喷洒茉莉酸甲酯和水杨酸甲酯的完整植物叶片中以及在通过叶柄切口供应来自每种编码蛋白C末端肽的离体叶片中差异表达。肽引发的PDF1.2和PR-1的表达在缺乏茉莉酸/乙烯和水杨酸途径的突变植物中以及在野生型植物中通过用二苯基碘鎓氯化物(过氧化氢产生的抑制剂)处理而被阻断。PROPEP1、PROPEP2和PROPEP3基因似乎在一个反馈回路中发挥作用,该回路放大了由病原体启动的防御信号通路。

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