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

被引:32
作者
Huang, Jianhua [1 ,2 ]
Sun, Yulin [2 ]
Orduna, Alberto R. [3 ]
Jetter, Reinhard [2 ]
Li, Xin [1 ,2 ]
机构
[1] Univ British Columbia, Michael Smith Labs, Vancouver, BC V6T 1Z4, Canada
[2] Univ British Columbia, Dept Bot, Vancouver, BC V6T 1Z4, Canada
[3] Univ British Columbia, Dept Chem, Vancouver, BC V6T 1Z1, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
plant immunity; salicylic acid; systemic acquired resistance; mediator; CDK8; MED12; CAMTA; transcriptional regulation; Arabidopsis thaliana; BINDING TRANSCRIPTION ACTIVATORS; GENE-EXPRESSION; DISEASE RESISTANCE; DEFENSE RESPONSES; FUNGAL PATHOGENS; PLANT IMMUNITY; ARABIDOPSIS; COMPLEX; SUBUNIT; JASMONATE;
D O I
10.1111/tpj.14278
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
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.
引用
收藏
页码:842 / 852
页数:11
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