Death don't have no mercy and neither does calcium:: Arabidopsis CYCLIC NUCLEOTIDE GATED CHANNEL2 and innate immunity
Death don't have no mercy and neither does calcium:: Arabidopsis CYCLIC NUCLEOTIDE GATED CHANNEL2 and innate immunity
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DOI：
10.1105/tpc.106.045096
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发表时间：
2007-03-01
期刊：
影响因子：
11.6
通讯作者：
Berkowitz, Gerald A.
中科院分区：
文献类型：
--
作者：
Ali, Rashid;Ma, Wei;Berkowitz, Gerald A.
植物对病原体感染的先天免疫反应包括一个优雅的信号通路，导致活性氧的产生和由此产生的超敏反应（HR）；最初感染部位周围组织的局部程序性细胞死亡限制了病原体的传播。胞质信号分子（包括Ca2+，一氧化氮[NO]，环核苷酸和钙调素）的真正交响乐被认为是HR信号的早期组成部分。然而，这些细胞质次级信使之间的具体相互作用及其在信号级联中的作用尚不清楚。在这里，我们报告了植物如何将对病原体的感知转化为导致先天免疫反应的信号级联的一些方面。我们发现拟南芥环核苷酸门控通道2 （CNGC2/DND1）将Ca2+传导到细胞中，并提供了一个将Ca2+电流与下游NO生产联系起来的模型。NO是激活植物先天免疫应答的重要信号分子。没有功能性CNGC2的植物缺乏这种细胞膜Ca2+电流，不显示HR；为突变体提供NO来补充这种表型。细菌病原体相关的分子模式激发子脂多糖激活CNGC Ca2+电流，这可能与由于细胞质Ca2+/钙调蛋白的积累而产生的NO有关。
Plant innate immune response to pathogen infection includes an elegant signaling pathway leading to reactive oxygen species generation and resulting hypersensitive response (HR); localized programmed cell death in tissue surrounding the initial infection site limits pathogen spread. A veritable symphony of cytosolic signaling molecules (including Ca2+, nitric oxide [NO], cyclic nucleotides, and calmodulin) have been suggested as early components of HR signaling. However, specific interactions among these cytosolic secondary messengers and their roles in the signal cascade are still unclear. Here, we report some aspects of how plants translate perception of a pathogen into a signal cascade leading to an innate immune response. We show that Arabidopsis thaliana CYCLIC NUCLEOTIDE GATED CHANNEL2 (CNGC2/DND1) conducts Ca2+ into cells and provide a model linking this Ca2+ current to downstream NO production. NO is a critical signaling molecule invoking plant innate immune response to pathogens. Plants without functional CNGC2 lack this cell membrane Ca2+ current and do not display HR; providing the mutant with NO complements this phenotype. The bacterial pathogen associated molecular pattern elicitor lipopolysaccharide activates a CNGC Ca2+ current, which may be linked to NO generation due to buildup of cytosolic Ca2+/calmodulin.