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介体激酶模块作为水杨酸积累和系统获得抗性的正调控因子。

The Mediator kinase module serves as a positive regulator of salicylic acid accumulation and systemic acquired resistance.

机构信息

Michael Smith Laboratories, University of British Columbia, Vancouver, BC, Canada, V6T 1Z4.

Department of Botany, University of British Columbia, Vancouver, BC, Canada, V6T 1Z4.

出版信息

Plant J. 2019 Jun;98(5):842-852. doi: 10.1111/tpj.14278. Epub 2019 Mar 25.

DOI:10.1111/tpj.14278
PMID:30739357
Abstract

In plants, the calmodulin-binding transcription activators (CAMTAs) are required for transcriptional regulation of abiotic and biotic stress responses. Among them, CAMTA3 in Arabidopsis has been intensively studied and shown to function redundantly with CAMTA1 and CAMTA2 to negatively regulate plant immunity. The camta1/2/3 triple mutant accordingly exhibits severe dwarfism due to autoimmunity. Here, through a suppressor screen using camta1/2/3 triple mutant, we found that a mutation in Cyclin-Dependent Kinase 8 (CDK8) partially suppresses the dwarfism and constitutive resistance phenotypes of camta1/2/3. CDK8 positively regulates steady-state salicylic acid (SA) levels and systemic required resistance (SAR). The expression of SA biosynthesis genes such as ICS1 and EDS5 is down-regulated in cdk8 mutants under uninfected conditions, suggesting that CDK8 contributes to the transcriptional regulation of these SA pathway genes. Knocking out another Mediator kinase module member MED12 yielded similar defects including decreased steady-state SA level and compromised SAR, suggesting that the whole Mediator kinase module contributes to the transcriptional regulation of SA levels and SAR.

摘要

在植物中,钙调素结合转录激活因子(CAMTAs)是参与非生物和生物胁迫反应转录调控所必需的。其中,拟南芥中的 CAMTA3 已被深入研究,并被证明与 CAMTA1 和 CAMTA2 冗余发挥作用,负调控植物免疫。camta1/2/3 三重突变体因此由于自身免疫而表现出严重的矮化。在这里,通过使用 camta1/2/3 三重突变体的抑制子筛选,我们发现细胞周期蛋白依赖性激酶 8(CDK8)的突变部分抑制了 camta1/2/3 的矮化和组成型抗性表型。CDK8 正向调控稳定态水杨酸(SA)水平和系统所需的抗性(SAR)。在未感染条件下,cdk8 突变体中 SA 生物合成基因如 ICS1 和 EDS5 的表达下调,表明 CDK8 有助于这些 SA 途径基因的转录调控。敲除另一个中介激酶模块成员 MED12 也会产生类似的缺陷,包括稳定态 SA 水平降低和 SAR 受损,表明整个中介激酶模块有助于 SA 水平和 SAR 的转录调控。

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