Arabidopsis DND2, a second cyclic nucleotide-gated ion channel gene for which mutation causes the "defense, no death" phenotype
Arabidopsis DND2, a second cyclic nucleotide-gated ion channel gene for which mutation causes the "defense, no death" phenotype
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DOI：
10.1094/mpmi.2004.17.5.511
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发表时间：
2004-05-01
影响因子：
3.5
通讯作者：
Bent, AF
中科院分区：
文献类型：
--
作者：
Jurkowski, GI;Smith, RK;Bent, AF
先前的突变屏幕鉴定出拟南芥DND1和DND2“防御，无死亡”突变体，它们表现出非基因抗性损失的过度反应（HR）细胞死亡的丧失。 DND1表型是由编码环状核苷酸门控（CNG）离子通道ATCNGC2的突变引起的。这项研究是DND2植物的特征。即使在表达AVRRPT2的曲丁氏菌的高滴度的情况下，DND2突变体中的大多数叶叶叶叶细胞也显示出没有HR。这些植物保留了强大的RPS2-，RPM1-或RPS4介导的丁香假单胞菌病原体生长的限制。突变的DND2植物还表现出对毒性P丁香病的宽光谱耐药性和组成型升高的水杨酸水平，以及与发病机理相关的（PR）基因表达。与野生型不同，对毒和无毒的P丁香响应的DND2植物表现出依赖水杨酸酯依赖性PR-1的表达升高，贾斯对月酸盐和依赖乙烯依赖性PDF1.2。将NAHG（+）（水杨酸盐羟化酶）引入DND2背景，该背景消除了水杨酸并引起其他防御改变，消除了组成型疾病的耐药性和PR基因的表达，但仅对HR-表型产生了较小的影响。基于地图的克隆表明DND2表型是由第二个CNG离子通道基因ATCNGC4突变引起的。因此，两个功能上非冗余的CNG离子通道中的任何一个都可能导致DND表型。 DND突变体为防御信号的解剖提供了独特的遗传背景。
A previous mutant screen identified Arabidopsis dnd1 and dnd2 "defense, no death" mutants, which exhibit loss of hypersensitive response (HR) cell death without loss of gene-for-gene resistance. The dnd1 phenotype is caused by mutation of the gene encoding cyclic nucleotide-gated (CNG) ion channel AtCNGC2. This study characterizes dnd2 plants. Even in the presence of high titers of Pseudomonas syringae expressing avrRpt2, most leaf mesophyll cells in the dnd2 mutant exhibited no HR. These plants retained strong RPS2-, RPM1-, or RPS4-mediated restriction of P. syringae pathogen growth. Mutant dnd2 plants also exhibited enhanced broad-spectrum resistance against virulent P syringae and constitutively elevated levels of salicylic acid, and pathogenesis-related (PR) gene expression. Unlike the wild type, dnd2 plants responding to virulent and avirulent P syringae exhibited elevated expression of both salicylate-dependent PR-1 and jasmonate and ethylene-dependent PDF1.2. Introduction of nahG(+) (salicylate hydroxylase) into the dnd2 background, which removes salicyllic acid and causes other defense alterations, eliminated constitutive disease resistance and PR gene expression but only weakly impacted the HR- phenotype. Map-based cloning revealed that dnd2 phenotypes are caused by mutation of a second CNG ion channel gene, AtCNGC4. Hence, loss of either of two functionally nonredundant CNG ion channels can cause dnd phenotypes. The dnd mutants provide a unique genetic background for dissection of defense signaling.