Perception of the Arabidopsis Danger Signal Peptide 1 Involves the Pattern Recognition Receptor AtPEPR1 and Its Close Homologue AtPEPR2
Perception of the Arabidopsis Danger Signal Peptide 1 Involves the Pattern Recognition Receptor AtPEPR1 and Its Close Homologue AtPEPR2
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DOI：
10.1074/jbc.m109.097394
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发表时间：
2010-04-30
影响因子：
4.8
通讯作者：
Hedrich, Rainer
中科院分区：
文献类型：
--
作者：
Krol, Elzbieta;Mentzel, Tobias;Hedrich, Rainer
质膜上的模式识别受体可以识别微生物相关的分子模式和内源性损伤相关的分子模式，为先天免疫提供了第一道防线。在植物中，富含亮氨酸的重复序列受体激酶（FLS2）和EFR （FLS2和EFR是鞭毛蛋白和延伸因子Tu的微生物相关分子模式受体）发挥了这一作用。在这里，我们研究了对损伤相关分子模式肽1 （AtPep1）的感知，这是一种早前发现的拟南芥内源性肽，可被富含亮氨酸的重复序列蛋白激酶PEPR1感知。通过抑制幼苗生长、诱导氧化爆发和诱导乙烯生物合成，我们发现野生型植物和pepr1和pepr2突变体对AtPep1及其同源物pepr2敏感，而双突变体pepr1/pepr2完全不敏感。作为我们研究的中心，我们提供了电生理学证据，证明在质膜水平上，AtPep1通过激活质膜阴离子通道触发受体依赖的瞬时去极化，而这种作用在双突变体pepr1/pepr2中不存在。在同源性筛选的基础上，双突变体对AtPep1的两个远同源物AtPep2和AtPep3也没有反应，这意味着PEPR1和PEPR2也对它们的感知负责。我们的发现为研究atpep1相关危险信号及其同源受体的生物学作用提供了一个基本框架。
Plasma membrane-borne pattern recognition receptors, which recognize microbe-associated molecular patterns and endogenous damage-associated molecular patterns, provide the first line of defense in innate immunity. In plants, leucine-rich repeat receptor kinases fulfill this role, as exemplified by FLS2 and EFR, the receptors for the microbe-associated molecular patterns flagellin and elongation factor Tu. Here we examined the perception of the damage-associated molecular pattern peptide 1 (AtPep1), an endogenous peptide of Arabidopsis identified earlier and shown to be perceived by the leucine-rich repeat protein kinase PEPR1. Using seedling growth inhibition, elicitation of an oxidative burst and induction of ethylene biosynthesis, we show that wild type plants and the pepr1 and pepr2 mutants, affected in PEPR1 and in its homologue PEPR2, are sensitive to AtPep1, but that the double mutant pepr1/pepr2 is completely insensitive. As a central body of our study, we provide electrophysiological evidence that at the level of the plasma membrane, AtPep1 triggers a receptor-dependent transient depolarization through activation of plasma membrane anion channels, and that this effect is absent in the double mutant pepr1/pepr2. The double mutant also fails to respond to AtPep2 and AtPep3, two distant homologues of AtPep1 on the basis of homology screening, implying that the PEPR1 and PEPR2 are responsible for their perception too. Our findings provide a basic framework to study the biological role of AtPep1-related danger signals and their cognate receptors.