ACD6, a novel ankyrin protein, is a regulator and an effector of salicylic acid signaling in the Arabidopsis Defense response
ACD6, a novel ankyrin protein, is a regulator and an effector of salicylic acid signaling in the Arabidopsis Defense response
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DOI：
10.1105/tpc.015412
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发表时间：
2003-10-01
期刊：
影响因子：
11.6
通讯作者：
Greenberg, JT
中科院分区：
文献类型：
--
作者：
Lu, H;Rate, DN;Greenberg, JT
先前报道的拟南芥显性功能获得突变体加速细胞死亡6 -1（acd 6 -1）显示自发细胞死亡和增强的抗病性。acd 6 -1还赋予对主要防御信号水杨酸（SA）的增加的响应性。为了进一步探讨ACD 6在防御反应中的作用，我们克隆并鉴定了该基因。ACD 6编码一种具有锚蛋白和跨膜区的新蛋白。它是高等植物中最大的未表征基因家族之一。ACD 6 mRNA的稳态基础表达需要光、SA和完整的SA信号通路。此外，ACD 6 mRNA水平增加，在系统的，未感染的组织的假单胞菌感染的植物，以及在植物与SA激动剂苯并噻唑（BTH）。一个新分离的ACD 6功能丧失突变体对BTH的反应较低，并且在P. dichloringae感染后SA水平降低，易感性增加。相反，过表达ACD 6的植物显示出适度增加的SA水平、增加的对烟草赤星病菌的抗性和BTH诱导的和/或低水平的自发细胞死亡。因此，ACD 6是针对毒性细菌的防御反应的必需的和剂量依赖性的激活剂，并且可以激活SA依赖性细胞死亡。
The previously reported Arabidopsis dominant gain-of-function mutant accelerated cell death6-1 (acd6-1) shows spontaneous cell death and increased disease resistance. acd6-1 also confers increased responsiveness to the major defense signal salicylic acid [SA). To further explore the role of ACD6 in the defense response, we cloned and characterized the gene. ACD6 encodes a novel protein with putative ankyrin and transmembrane regions. It is a member of one of the largest uncharacterized gene families in higher plants. Steady state basal expression of ACD6 mRNA required light, SA, and an intact SA signaling pathway. Additionally, ACD6 mRNA levels were increased in the systemic, uninfected tissue of Pseudomonas syringae-infected plants as well as in plants treated with the SA agonist benzothiazole (BTH). A newly isolated ACD6 loss-of-function mutant was less responsive to BTH and upon P. syringae infection had reduced SA levels and increased susceptibility. Conversely, plants overexpressing ACD6 showed modestly increased SA levels, increased resistance to P. syringae, and BTH-inducible and/or a low level of spontaneous cell death. Thus, ACD6 is a necessary and dose-dependent activator of the defense response against virulent bacteria and can activate SA-dependent cell death.