CDK抑制子（ICK）通过茉莉酸信号途径调控植物抗病性的研究

Cyclin-dependent kinase (CDK) inhibitors play a pivotal role in cell cycle regulation. The mammalian CDK inhibitors have received considerable attention and have been investigated extensively because of their implications in human diseases particularly in cancer. However, little is known about whether plant CDK inhibitors (ICKs) have any role in plant disease resistance. In our previous study, we had constructed an Arabidopsis quintuple mutant ick1 ick2 ick5 ick6 ick7 (ick1/2/5/6/7), in which five ICK genes were disrupted by T-DNA insertions, and found that the resistance to Sclerotinia sclerotiorum and Botrytis cinerea was significantly increased compared to the wild type. Genome-wide gene expression profiling of ick1/2/5/6/7, ICK1OE and wild-type Arabidopsis lines indicated that CDK were involved in the regulation of jasmonic acid signaling pathway. Based on these findings, we proposed a putative model to explain the mechanism regarding how ICKs were participated in plant pathogen resistance: ICKs inhibit the kinase activity of CDKs, and CDKs catalyze the phosphorylation of JAZs; after phosphorylated, JAZs release the Myc2 transcriptional factor, as result, the expressions of JA-responsive genes are up-regulated and the plant resistance to pathogen is increased. In this study, we are trying to validate this putative model using biochemical and molecular techniques. This model will integrate the cell cycle regulation machinery with the jasmonic acid signaling and plant pathogen resistance.

周期蛋白依赖性激酶（CDK）抑制子在细胞周期调控中起重要作用。哺乳动物的CDK抑制子由于与疾病尤其是癌症相关而受到深入的研究。然而，对植物CDK抑制子（ICK）是否参与植物抗病还知之甚少。前期研究中，我们构建了五个ICK基因被敲除的拟南芥突变体ick1/2/5/6/7并发现它的菌核病和灰霉病抗性较野生型明显增强；ick1/2/5/6/7, ICK1OE和野生型拟南芥的表达谱分析显示CDK参与了茉莉酸（JA）信号途径的调节。基于此，我们提出了一个假设机制阐述ICK参与植物抗病调控的机理：ICK抑制CDK激酶活性，而CDK则磷酸化JAZ使其释放MYC2转录因子，从而开启茉莉酸应答基因的表达，导致植物的抗病性增强。本研究试图通过生化和分子生物学手段对这个假设机理的关键模型进行验证。这个模型将把细胞周期调控和茉莉酸信号途径、植物抗病性联系起来。

周期蛋白依赖性激酶（CDK）抑制子在细胞周期调控中起重要作用。哺乳动物的CDK抑制子由于与疾病尤其是癌症相关而受到深入的研究。然而，对植物CDK抑制子（ICK）是否参与植物抗病还知之甚少。前期研究中，我们构建了五个ICK基因被敲除的拟南芥突变体ick1/2/5/6/7并发现它的菌核病和灰霉病抗性较野生型明显增强；ick1/2/5/6/7, ICK1OE和野生型拟南芥的表达谱分析显示CDK参与了茉莉酸（JA）信号途径的调节。基于此，我们提出了一个假设机制阐述ICK参与植物抗病调控的机理：ICK抑制CDK激酶活性，而CDK则磷酸化JAZ使其释放MYC2转录因子，从而开启茉莉酸应答基因的表达，导致植物的抗病性增强。本项目开展实验，验证了如下要点：1）证实了CDK激酶复合体能够磷酸化JAZ蛋白。2）证实了JAZ蛋白磷酸化之后与MYC2的结合能力减弱；3）证实了JAZ蛋白磷酸化后对MYC2转录因子的抑制作为用减弱，从而上调了MYC2下游调控基因的表达，激活了JA调控途径，提高了植物的抗病性和抗虫能力。本项目中的发现首次把细胞周期调控核心因子与植物的激素调控途径联系起来；调控CDK激酶活性可以显著提高植物抗性在作物遗传育种中更有应用意义。