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拟南芥Cullin1中的点突变揭示了其在茉莉酸反应中的重要作用。

Point mutations in Arabidopsis Cullin1 reveal its essential role in jasmonate response.

作者信息

Ren Chunmei, Pan Jianwei, Peng Wen, Genschik Pascal, Hobbie Lawrence, Hellmann Hanjo, Estelle Mark, Gao Bida, Peng Jinrong, Sun Chuanqing, Xie Daoxin

机构信息

College of Bio-Safety Science and Technology, Hunan Agricultural University, Changsha, 410128 China.

出版信息

Plant J. 2005 May;42(4):514-24. doi: 10.1111/j.1365-313X.2005.02394.x.

DOI:10.1111/j.1365-313X.2005.02394.x
PMID:15860010
Abstract

The SKP1-Cullin/Cdc53-F-box protein ubiquitin ligases (SCF) target many important regulatory proteins for degradation and play vital roles in diverse cellular processes. In Arabidopsis there are 11 Cullin members (AtCUL). AtCUL1 was demonstrated to assemble into SCF complexes containing COI1, an F-box protein required for response to jasmonates (JA) that regulate plant fertility and defense responses. It is not clear whether other Cullins also associate with COI1 to form SCF complexes, thus, it is unknown whether AtCUL1, or another Cullin that assembles into SCF(COI1) (even perhaps two or more functionally redundant Cullins), plays a major role in JA signaling. We present genetic and physiological data to directly demonstrate that AtCUL1 is necessary for normal JA responses. The homozygous AtCUL1 mutants axr6-1 and axr6-2, the heterozygous mutants axr6/AXR6, and transgenic plants expressing mutant AtCUL1 proteins containing a single amino acid substitution from phenylalanine-111 to valine, all exhibit reduced responses to JA. We also demonstrate that ax6 enhances the effect of coi1 on JA responses, implying a genetic interaction between COI1 and AtCUL1 in JA signaling. Furthermore, we show that the point mutations in AtCUL1 affect the assembly of COI1 into SCF, thus attenuating SCF(COI1) formation.

摘要

SKP1-库林/Cdc53-F盒蛋白泛素连接酶(SCF)靶向许多重要的调节蛋白进行降解,并在多种细胞过程中发挥关键作用。在拟南芥中,有11个库林成员(AtCUL)。AtCUL1被证明可组装成包含COI1的SCF复合物,COI1是一种F盒蛋白,是茉莉酸(JA)反应所必需的,而茉莉酸可调节植物育性和防御反应。目前尚不清楚其他库林是否也与COI1结合形成SCF复合物,因此,AtCUL1或另一种组装成SCF(COI1)的库林(甚至可能是两个或更多功能冗余的库林)是否在JA信号传导中起主要作用尚不清楚。我们提供了遗传和生理学数据,直接证明AtCUL1是正常JA反应所必需的。纯合AtCUL1突变体axr6-1和axr6-2、杂合突变体axr6/AXR6以及表达含有从苯丙氨酸-111到缬氨酸的单个氨基酸取代的突变AtCUL1蛋白的转基因植物,均表现出对JA的反应降低。我们还证明ax6增强了coi1对JA反应的影响,这意味着COI1和AtCUL1在JA信号传导中存在遗传相互作用。此外,我们表明AtCUL1中的点突变影响COI1组装成SCF,从而减弱SCF(COI1)的形成。

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