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首页> 外文期刊>The Plant Cell >ETHYLENE-INSENSITIVE3 is a senescence-associated gene that accelerates age-dependent leaf senescence by directly repressing miR164 transcription in Arabidopsis.
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ETHYLENE-INSENSITIVE3 is a senescence-associated gene that accelerates age-dependent leaf senescence by directly repressing miR164 transcription in Arabidopsis.

机译:ETHYLENE-INSENSITIVE3是与衰老相关的基因,可通过直接抑制拟南芥中的miR164转录来加速依赖年龄的叶片衰老。

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Numerous endogenous and environmental signals regulate the intricate and highly orchestrated process of plant senescence. Ethylene is a well-known inducer of senescence, including fruit ripening and flower and leaf senescence. However, the underlying molecular mechanism of ethylene-induced leaf senescence remains to be elucidated. Here, we examine ETHYLENE-INSENSITIVE3 (EIN3), a key transcription factor in ethylene signaling, and find that EIN3 is a functional senescence-associated gene. Constitutive overexpression or temporary activation of EIN3 is sufficient to accelerate leaf senescence symptoms. Conversely, loss of EIN3 and EIN3-Like1 (its close homolog) function leads to a delay in age-dependent and ethylene-, jasmonic acid-, or dark-induced leaf senescence. We further found that EIN3 acts downstream of ORESARA2 (ORE2)/ORE3/EIN2 to repress miR164 transcription and upregulate the transcript levels of ORE1/NAC2, a target gene of miR164. EIN3 directly binds to the promoters of microRNA164 (miR164), and this binding activity progressively increases during leaf ageing. Genetic analysis revealed that overexpression of miR164 or knockout of ORE1/NAC2 represses EIN3-induced early-senescence phenotypes. Collectively, our study defines a continuation of the signaling pathway involving EIN2-EIN3-miR164-NAC2 in regulating leaf senescence and provides a mechanistic insight into how ethylene promotes the progression of leaf senescence in Arabidopsis thaliana.
机译:许多内源性和环境信号调节着植物衰老过程的复杂性和高度协调性。乙烯是众所周知的衰老诱导剂,包括果实成熟和花朵和叶子衰老。然而,乙烯诱导的叶片衰老的潜在分子机制仍有待阐明。在这里,我们检查了乙烯信号传导中的关键转录因子ETHENSENE-INSENSITIVE3(EIN3),并发现EIN3是功能性衰老相关基因。 EIN3的组成型过表达或暂时激活足以加速叶片衰老症状。相反,EIN3和EIN3-Like1(其紧密同源)功能的丧失会导致年龄依赖性和乙烯,茉莉酸或深色诱导的叶片衰老延迟。我们进一步发现,EIN3在ORESARA2(ORE2)/ ORE3 / EIN2的下游起作用,以抑制miR164转录并上调ORE1 / NAC2(miR164的靶基因)的转录水平。 EIN3直接与microRNA164(miR164)的启动子结合,并且这种结合活性在叶片老化过程中逐渐增加。遗传分析表明,miR164的过表达或ORE1 / NAC2的敲除可抑制EIN3诱导的早期衰老表型。总的来说,我们的研究定义了涉及EIN2-EIN3-miR164-NAC2的信号通路在调节叶片衰老中的延续,并提供了有关乙烯如何促进拟南芥叶片衰老进程的机制性见解。

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