The eer5 mutation, which affects a novel proteasome-related subunit, indicates a prominent role for the COP9 signalosome in resetting the ethylene-signaling pathway in Arabidopsis
The eer5 mutation, which affects a novel proteasome-related subunit, indicates a prominent role for the COP9 signalosome in resetting the ethylene-signaling pathway in Arabidopsis
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DOI：
10.1111/j.1365-313x.2008.03521.x
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发表时间：
2008-08-01
期刊：
影响因子：
7.2
通讯作者：
Larsen, Paul B.
中科院分区：
文献类型：
--
作者：
Christians, Matthew J.;Robles, Linda M.;Larsen, Paul B.
分离并鉴定了拟南芥突变体eer5-1，该突变体在黄化幼苗中对乙烯的反应增强，包括对乙烯的超敏感和极度夸张的反应。与其他已鉴定的突变体一样，eer5-1反应表型的增强与未能诱导适当的乙烯调节基因亚群相关，这表明适当的乙烯反应基因表达对于重置乙烯反应途径是必要的。eer5-1代表了一种突变，该突变导致先前未表征的基因中的氨基酸替换，该基因编码具有PAM[蛋白酶体COP9起始因子（PCI/PINT）相关模块]结构域的蛋白质，类似于COP9信号体（CSN）成分中的结构域。遗传分析表明，eer5突变体表型的表现完全依赖于乙烯信号，因为ein2-5 eer5-1双突变体在饱和乙烯浓度下与ein2-5无法区分。相比之下，EIN3 -1 EER5 -1双突变体表现出乙烯响应增强的特征，这表明EER5独立于EIN3调节乙烯信号。对EER5蛋白的分析表明，它与EIN2的c端和CSN相互作用，表明EER5作为EIN2和靶蛋白修饰或降解之间的桥梁，包括一组转录抑制因子，作为乙烯信号传导期间或之后重置机制的一部分。
An Arabidopsis mutant, eer5-1, which has an enhanced ethylene response in etiolated seedlings, including hypersensitivity and extreme exaggeration of response to ethylene, was isolated and characterized. As with other identified eer mutants, the enhanced response phenotype of eer5-1 was correlated with failure to induce appropriately a subset of ethylene-regulated genes, suggesting that proper ethylene-responsive gene expression is necessary for resetting the ethylene response pathway. eer5-1 represents a mutation that causes an amino acid substitution in a previously uncharacterized gene, which encodes a protein with a PAM [proteasome COP9 initiation factor (PCI/PINT)-associated module] domain similar to those found in components of the COP9 signalosome (CSN). Genetic analysis shows that manifestation of the eer5 mutant phenotype is solely dependent on ethylene signaling, as the ein2-5 eer5-1 double mutant was indistinguishable from ein2-5 in the presence of saturating ethylene concentrations. In contrast, the ein3-1 eer5-1 double mutant displayed characteristics of an enhanced ethylene response, and this suggests that EER5 regulates ethylene signaling independently of EIN3. Analysis of the EER5 protein indicates that it interacts with the C-terminus of EIN2 and with the CSN, suggesting that EER5 serves as a bridge between EIN2 and the modification or degradation of target proteins, including a proposed group of transcriptional repressors, as part of a resetting mechanism during or following ethylene signaling.