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生长素响应因子

Auxin response factors.

作者信息

Chandler John William

机构信息

Institute of Developmental Biology, University of Cologne, Cologne Biocenter, Zuelpicher Strasse 47b, Cologne, D-50674, Germany.

出版信息

Plant Cell Environ. 2016 May;39(5):1014-28. doi: 10.1111/pce.12662. Epub 2016 Jan 23.

DOI:10.1111/pce.12662
PMID:26487015
Abstract

Auxin signalling involves the activation or repression of gene expression by a class of auxin response factor (ARF) proteins that bind to auxin response elements in auxin-responsive gene promoters. The release of ARF repression in the presence of auxin by the degradation of their cognate auxin/indole-3-acetic acid repressors forms a paradigm of transcriptional response to auxin. However, this mechanism only applies to activating ARFs, and further layers of complexity of ARF function and regulation are being revealed, which partly reflect their highly modular domain structure. This review summarizes our knowledge concerning ARF binding site specificity, homodimer and heterodimer multimeric ARF association and cooperative function and how activator ARFs activate target genes via chromatin remodelling and evolutionary information derived from phylogenetic comparisons from ARFs from diverse species. ARFs are regulated in diverse ways, and their importance in non-auxin-regulated pathways is becoming evident. They are also embedded within higher-order transcription factor complexes that integrate signalling pathways from other hormones and in response to the environment. The ways in which new information concerning ARFs on many levels is causing a revision of existing paradigms of auxin response are discussed.

摘要

生长素信号传导涉及一类生长素响应因子(ARF)蛋白对基因表达的激活或抑制,这些蛋白与生长素响应基因启动子中的生长素响应元件结合。在生长素存在的情况下,通过其同源生长素/吲哚 - 3 - 乙酸阻遏物的降解来释放ARF抑制,形成了对生长素转录反应的范例。然而,这种机制仅适用于激活型ARF,并且ARF功能和调控的更多复杂层面正在被揭示,这部分反映了它们高度模块化的结构域结构。本综述总结了我们关于ARF结合位点特异性、同型二聚体和异型二聚体多聚体ARF关联及协同功能的知识,以及激活型ARF如何通过染色质重塑激活靶基因,还有从不同物种的ARF系统发育比较中获得的进化信息。ARF以多种方式受到调控,它们在非生长素调控途径中的重要性正变得明显。它们还嵌入在更高层次的转录因子复合物中,这些复合物整合了来自其他激素的信号通路并响应环境。本文讨论了关于ARF的多层面新信息如何导致对现有生长素响应范例的修订。

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