The Arabidopsis-accelerated cell death gene ACD2 encodes red chlorophyll catabolite reductase and suppresses the spread of disease symptoms.
The Arabidopsis-accelerated cell death gene ACD2 encodes red chlorophyll catabolite reductase and suppresses the spread of disease symptoms.
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DOI：
10.1073/pnas.98.2.771
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发表时间：
2001-01
影响因子：
11.1
通讯作者：
Jennifer Mach;Andrea R. Castillo;Rebecca Hoogstraten;Jean T. Greenberg
中科院分区：
文献类型：
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作者：
Jennifer Mach;Andrea R. Castillo;Rebecca Hoogstraten;Jean T. Greenberg
拟南芥的加速细胞死亡2（acd 2）突变体在没有病原体感染的情况下具有自发扩散的细胞死亡损伤和防御的组成性激活。acd 2植物中的病变形成可以由细菌毒素冠菌素通过光依赖性过程触发。acd 2植物中冠状病毒素引发的和自发的病斑扩散也需要蛋白质翻译，这表明细胞死亡是通过一个主动过程发生的。我们已经克隆了ACD 2基因;其预测产物显示出与红色叶绿素分解代谢物还原酶的显著和广泛的相似性，所述还原酶催化叶绿素的卟啉组分的分解中的一个步骤[Wüthrich，K. L.，博韦湖，亨齐格，体育，唐尼森岛S. & Hörtensteiner，S.（2000）Plant J.21，189-198]。与此一致，ACD 2蛋白含有预测的叶绿体转运肽，在体内加工，并在亚细胞分级分离实验中用叶绿体级分纯化。在发育的某些阶段，ACD 2蛋白也与线粒体组分一起纯化。我们推测acd 2植物的细胞死亡是由叶绿素分解产物的积累引起的。这种催化剂可能是细胞死亡的特异性触发剂，或者它们可能通过吸收光和释放产生自由基的电子的能力诱导细胞损伤。响应于假单胞菌的感染，表达过量ACD 2蛋白的转基因植物显示出减少的疾病症状，但不减少细菌的生长。因此，叶绿素的分解产物可能会放大疾病的症状，包括细胞死亡和变黄。我们认为，经济上重要的植物过表达ACD 2也可能表现出对病原体的耐受性增加，并可能有助于提高作物产量。
accelerated cell death 2 (acd2) mutants of Arabidopsis have spontaneous spreading cell death lesions and constitutive activation of defenses in the absence of pathogen infection. Lesion formation in acd2 plants can be triggered by the bacterial toxin coronatine through a light-dependent process. Coronatine-triggered and spontaneous lesion spreading in acd2 plants also requires protein translation, indicating that cell death occurs by an active process. We have cloned the ACD2 gene; its predicted product shows significant and extensive similarity to red chlorophyll catabolite reductase, which catalyzes one step in the breakdown of the porphyrin component of chlorophyll [Wüthrich, K. L., Bovet, L., Hunziger, P. E., Donnison, I. S. & Hörtensteiner, S. (2000) Plant J. 21, 189-198]. Consistent with this, ACD2 protein contains a predicted chloroplast transit peptide, is processed in vivo, and purifies with the chloroplast fraction in subcellular fractionation experiments. At some stages of development, ACD2 protein also purifies with the mitochondrial fraction. We hypothesize that cell death in acd2 plants is caused by the accumulation of chlorophyll breakdown products. Such catabolites might be specific triggers for cell death or they might induce cellular damage through their ability to absorb light and emit electrons that generate free radicals. In response to infection by Pseudomonas syringae, transgenic plants expressing excess ACD2 protein show reduced disease symptoms but not reduced growth of bacteria. Thus, breakdown products of chlorophyll may act to amplify the symptoms of disease, including cell death and yellowing. We suggest that economically important plants overexpressing ACD2 might also show increased tolerance to pathogens and might be useful for increasing crop yields.