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首页> 外文期刊>The Plant Cell >Arabidopsis CULLIN4 forms an E3 ubiquitin ligase with RBX1 and the CDD complex in mediating light control of development.
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Arabidopsis CULLIN4 forms an E3 ubiquitin ligase with RBX1 and the CDD complex in mediating light control of development.

机译:拟南芥CULLIN4与RBX1和CDD复合物形成E3泛素连接酶,介导发育的光控制。

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摘要

Repression of photomorphogenesis in Arabidopsis thaliana requires activity of the COP9 signalosome (CSN), CDD, and COP1 complexes, but how these three complexes work in concert to accomplish this important developmental switch has remained unknown. Here, we demonstrate that Arabidopsis CULLIN4 (CUL4) associates with the CDD complex and a common catalytic subunit to form an active E3 ubiquitin ligase both in vivo and in vitro. The partial loss of function of CUL4 resulted in a constitutive photomorphogenic phenotype with respect to morphogenesis and light-regulated gene expression. Furthermore, CUL4 exhibits a synergistic genetic interaction with COP10 and DET1. Therefore, this CUL4-based E3 ligase is essential for the repression of photomorphogenesis. This CUL4-based E3 ligase appears to associate physically with COP1 E3 ligase and positively regulates the COP1-dependent degradation of photomorphogenesis-promoting transcription factors, whereas the CSN controls the biochemical modification of CUL4 essential for E3 activity. Thus, this study suggests a biochemical activity connection between CSN and CDD complexes in their cooperation with COP1 in orchestrating the repression of photomorphogenesis..
机译:拟南芥中光形态发生的抑制需要COP9信号小体(CSN),CDD和COP1复合物的活性,但是这三种复合物如何协同工作以实现这一重要的发育转换仍是未知的。在这里,我们证明了拟南芥CULLIN4(CUL4)与CDD复合物和一个共同的催化亚基缔合,在体内和体外均形成活性E3泛素连接酶。在形态发生和光调节基因表达方面,CUL4功能的部分丧失导致组成型光形态发生表型。此外,CUL4与COP10和DET1表现出协同的遗传相互作用。因此,这种基于CUL4的E3连接酶对于抑制光形态发生至关重要。这种基于CUL4的E3连接酶似乎在物理上与COP1 E3连接酶缔合,并正调控光合作用促进转录因子的COP1依赖性降解,而CSN控制着E3活性必需的CUL4的生化修饰。因此,这项研究表明CSN和CDD配合物在与COP1协同调控光形态发生的过程中具有生化活性联系。

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