Constitutive salicylic acid-dependent signaling in cpr1 and cpr6 mutants requires PAD4

Constitutive salicylic acid-dependent signaling in cpr1 and cpr6 mutants requires PAD4
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DOI:
10.1046/j.1365-313x.2001.2641040.x
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发表时间:
2001-05-01
期刊:
影响因子:
7.2
通讯作者:
Glazebrook, J
Glazebrook, J
中科院分区:
生物学1区
文献类型:
--
作者:
Jirage, D;Zhou, N;Glazebrook, J

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水杨酸(SA)依赖的信号控制一系列植物防御机制的激活,这些机制对于抵抗各种微生物病原体是重要的。许多具有SA依赖信号的拟南芥突变体已经被分离出来。我们使用双突变分析来确定Pad4、cpr1、cpr5、cpr6、dnd1和dnd2突变在导致SA依赖的防御基因表达和抗病性激活的信号转导网络中的相对位置。PAD4突变导致SA不能在某些病原体的侵染下积累,而其他突变则导致SA、防御基因的表达和抗性的结构性高水平。构建了cpr7 PAD4、cpr5 PAD4、cpr6 PAD4、dnd1 PAD4和dnd2 PAD4双突变体,并测定了它们的体型、自发性病变的存在、对丁香假单胞菌和寄生轮孢菌的抗性、SA水平、PAD4 PR-I和PDF1.2的表达以及Camalexin的积累。我们发现cpr1和cpr6突变对SA依赖基因表达的影响完全依赖于PAD4功能。相反,在模拟病变的突变体cpr5中,SA的积累部分不依赖于PAD4,而在dnd1和dnd2突变体中,SA的积累完全不依赖于PAD4。提出了一个描述信号转导网络中可能的活动安排的模型。
Salicylic acid (SA)-dependent signaling controls activation of a set of plant defense mechanisms that are important for resistance to a variety of microbial pathogens. Many Arabidopsis mutants that display altered SA-dependent signaling have been isolated. We used double mutant analysis to determine the relative positions of the pad4, cpr1, cpr5, cpr6, dnd1 and dnd2 mutations in the signal transduction network leading to SA-dependent activation of defense gene expression and disease resistance. The pad4 mutation causes failure of SA accumulation in response to infection by certain pathogens, while the other mutations cause constitutively high levels of SA, defense gene expression and resistance. The cpr7 pad4, cpr5 pad4, cpr6 pad4, dnd1 pad4 and dnd2 pad4 double mutants were constructed and assayed for stature, presence of spontaneous lesions, resistance to Pseudomonas syringae and Peronospora parasitica, SA levels, expression of PAD4 PR-I and PDF1.2 and accumulation of camalexin. We found that the effects of the cpr1 and cpr6 mutations on SA-dependent gene expression are completely dependent on PAD4 function. In contrast, SA accumulation in the lesion-mimic mutant cpr5 is partially PAD4-independent, while in dnd1 and dnd2 mutants it is completely PAD4-independent. A model describing a possible arrangement of activities in the signal transduction network is presented.