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拟南芥细胞周期蛋白依赖性激酶C复合物在花椰菜花叶病毒感染、植物生长和发育中的作用。

Roles of Arabidopsis cyclin-dependent kinase C complexes in cauliflower mosaic virus infection, plant growth, and development.

作者信息

Cui Xiaofeng, Fan Baofang, Scholz James, Chen Zhixiang

机构信息

Department of Botany and Plant Pathology, Purdue University, West Lafayette, Indiana 47907-2054, USA.

出版信息

Plant Cell. 2007 Apr;19(4):1388-402. doi: 10.1105/tpc.107.051375. Epub 2007 Apr 27.

DOI:10.1105/tpc.107.051375
PMID:17468259
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1913762/
Abstract

The C-terminal domain (CTD) of RNA polymerase II is phosphorylated during the transcription cycle by three cyclin-dependent kinases (CDKs): CDK7, CDK8, and CDK9. CDK9 and its interacting cyclin T partners belong to the positive transcription elongation factor b (P-TEFb) complexes, which phosphorylate the CTD to promote transcription elongation. We report that Arabidopsis thaliana CDK9-like proteins, CDKC;1 and CDKC;2, and their interacting cyclin T partners, CYCT1;4 and CYCT1;5, play important roles in infection with Cauliflower mosaic virus (CaMV). cdkc;2 and cyct1;5 knockout mutants are highly resistant and cdkc;2 cyct1;5 double mutants are extremely resistant to CaMV. The mutants respond normally to other types of plant viruses that do not replicate by reverse transcription. Expression of a reporter gene driven by the CaMV 35S promoter is markedly reduced in the cdkc;2 and cyct1;5 mutants, indicating that the kinase complexes are important for transcription from the viral promoter. Loss of function of CDKC;1/CDKC;2 or CYCT1;4/CYCT1;5 results in complete resistance to CaMV as well as altered leaf and flower growth, trichome development, and delayed flowering. These results establish Arabidopsis CDKC kinase complexes as important host targets of CaMV for transcriptional activation of viral genes and critical regulators of plant growth and development.

摘要

RNA聚合酶II的C末端结构域(CTD)在转录周期中被三种细胞周期蛋白依赖性激酶(CDK)磷酸化:CDK7、CDK8和CDK9。CDK9及其相互作用的细胞周期蛋白T伴侣属于正转录延伸因子b(P-TEFb)复合物,该复合物使CTD磷酸化以促进转录延伸。我们报道,拟南芥中类似CDK9的蛋白CDKC;1和CDKC;2,及其相互作用的细胞周期蛋白T伴侣CYCT1;4和CYCT1;5,在花椰菜花叶病毒(CaMV)感染中发挥重要作用。cdkc;2和cyct1;5敲除突变体对CaMV具有高度抗性,而cdkc;2 cyct1;5双突变体对CaMV具有极强的抗性。这些突变体对其他非通过逆转录复制的植物病毒类型反应正常。由CaMV 35S启动子驱动的报告基因在cdkc;2和cyct1;5突变体中的表达显著降低,表明该激酶复合物对病毒启动子的转录很重要。CDKC;1/CDKC;2或CYCT1;4/CYCT1;5功能丧失导致对CaMV完全抗性,以及叶片和花朵生长改变、毛状体发育和开花延迟。这些结果确立了拟南芥CDKC激酶复合物是CaMV转录激活病毒基因的重要宿主靶点以及植物生长和发育的关键调节因子。

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