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细胞周期蛋白依赖性激酶8通过激活WRI1转录正向调控油脂合成。

CYCLIN-DEPENDENT KINASE 8 positively regulates oil synthesis by activating WRINKLED1 transcription.

作者信息

Zhai Zhiyang, Blanford Jantana K, Cai Yingqi, Sun Jing, Liu Hui, Shi Hai, Schwender Jorg, Shanklin John

机构信息

Department of Biology, Brookhaven National Laboratory, Building 463, 50 Bell Ave, Upton, NY, 11973, USA.

出版信息

New Phytol. 2023 Apr;238(2):724-736. doi: 10.1111/nph.18764. Epub 2023 Feb 16.

Abstract

CYCLIN-DEPENDENT KINASE 8 (CDK8), a component of the kinase module of the Mediator complex in Arabidopsis, is involved in many processes, including flowering, plant defense, drought, and energy stress responses. Here, we investigated cdk8 mutants and CDK8-overexpressing lines to evaluate whether CDK8 also plays a role in regulating lipid synthesis, an energy-demanding anabolism. Quantitative lipid analysis demonstrated significant reductions in lipid synthesis rates and lipid accumulation in developing siliques and seedlings of cdk8, and conversely, elevated lipid contents in wild-type seed overexpressing CDK8. Transactivation assays show that CDK8 is necessary for maximal transactivation of the master seed oil activator WRINKLED1 (WRI1) by the seed maturation transcription factor ABSCISIC ACID INSENSITIVE3, supporting a direct regulatory role of CDK8 in oil synthesis. Thermophoretic studies show GEMINIVIRUS REP INTERACTING KINASE1, an activating kinase of KIN10 (a catalytic subunit of SUCROSE NON-FERMENTING1-RELATED KINASE1), physically interacts with CDK8, resulting in its phosphorylation and degradation in the presence of KIN10. This work defines a mechanism whereby, once activated, KIN10 downregulates WRI1 expression and suppresses lipid synthesis via promoting the degradation of CDK8. The KIN10-CDK8-dependent regulation of lipid synthesis described herein is additional to our previously reported KIN10-dependent phosphorylation and degradation of WRI1.

摘要

细胞周期蛋白依赖性激酶8(CDK8)是拟南芥中介体复合物激酶模块的一个组成部分,参与许多过程,包括开花、植物防御、干旱和能量应激反应。在这里,我们研究了cdk8突变体和CDK8过表达系,以评估CDK8是否也在调节脂质合成(一种需要能量的合成代谢)中发挥作用。定量脂质分析表明,cdk8发育中的角果和幼苗的脂质合成速率和脂质积累显著降低,相反,过表达CDK8的野生型种子中的脂质含量升高。反式激活分析表明,CDK8是种子成熟转录因子脱落酸不敏感3对主种子油激活剂皱叶1(WRI1)进行最大反式激活所必需的,这支持了CDK8在油脂合成中的直接调节作用。热泳研究表明,双生病毒REP相互作用激酶1(KIN10的激活激酶,KIN10是蔗糖非发酵1相关激酶1的催化亚基)与CDK8发生物理相互作用,导致其在KIN10存在的情况下发生磷酸化和降解。这项工作定义了一种机制,即一旦被激活,KIN10通过促进CDK8的降解来下调WRI1的表达并抑制脂质合成。本文所述的KIN10-CDK8依赖性脂质合成调节是我们先前报道的KIN10依赖性WRI1磷酸化和降解之外的。

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