CDK8作为中介因子复合体中的一个重要成员，已知参与调控植物花器官发育和抵御病原菌入侵等过程。然而它在重要植物激素信号转导途径和非生物胁迫应答中的功能尚不明确。我们近期研究发现CDK8的功能缺失明显降低植物对ABA的敏感性，却增加叶片失水速率和对干旱胁迫的敏感性。质谱分析CDK8在植物体内的结合蛋白时发现CDK8和SnRK2.6共存于一个蛋白复合体，酵母双杂交和荧光素酶互补实验显示CDK8与SnRK2.2/2.3/2.6确实存在互作，并发现CDK8的突变明显抑制了多个ABA响应基因的诱导表达。本项目拟重点研究CDK8与SnRK2.2/2.3/2.6之间的互作调节机制，鉴定CDK8的磷酸化底物，并解析CDK8和SnRK2.2/2.3/2.6共同和特异调控的下游基因。该研究有望揭示CDK8调控ABA信号转导通路和干旱胁迫应答机制，并有助于发现参与调控ABA信号通路下游基因转录的新途径。

As an important member of mediator complex, CDK8 is known to be involved in the regulation of flower organ development and resistance to pathogen invasion in plants. However, the roles of CDK8 in plant hormone signal transduction pathways and abiotic stress responses remain unclear. We recently found that cdk8 mutants showed reduced sensitivity to ABA, faster water loss and increased sensitivity to drought stress. We further used mass spectrometry approach to study the functional complex components of CDK8 and revealed that CDK8 and SnRK2.6 exist in a protein complex. Yeast two-hybrid (Y2H) and luciferase complementation imaging (LCI) experiments demonstrated that CDK8 can interact with SnRK2.2/2.3/2.6. Moreover, several ABA induced gene expressions were suppressed in cdk8 mutants. This project intends to illustrate the interactions and regulatory mechanism between CDK8 and SnRK2.2/2.3/2.6, identify the phosphorylated substrate of CDK8, and reveal the downstream and specific target genes of CDK8 and SnRK2.2/2.3/2.6. This study will uncover the molecular mechanism by which CDK8 regulates ABA signaling transduction and drought stress response, and will also help identify new pathways that regulate the transcription of downstream genes in the ABA signaling pathway.