Control of jasmonate biosynthesis and senescence by miR319 targets.
Control of jasmonate biosynthesis and senescence by miR319 targets.
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MiR319靶标对茉莉酸盐的生物合成和衰老。
DOI：
10.1371/journal.pbio.0060230
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发表时间：
2008-09-23
期刊：
影响因子：
9.8
通讯作者：
Weigel, Detlef
中科院分区：
文献类型：
--
作者：
Schommer, Carla;Palatnik, Javier F.;Aggarwal, Pooja;Chetelat, Aurore;Cubas, Pilar;Farmer, Edward E.;Nath, Utpal;Weigel, Detlef
在鉴定植物microRNA的靶标方面已经取得了相当大的进展，其中许多microRNA调节编码参与发育的转录因子的mRNA的稳定性或翻译。在大多数情况下，它是未知的，但是，直接转录靶介导的microRNA调节转录因子的下游效应。我们发现了一个由miR 319调控的TCP（TEOSINTE BRANCHED/CYCLOIDEA/PCF）转录因子基因进化枝控制的新过程。与其他miRNA靶点（其中几个调节激素反应）相反，TCP控制激素茉莉酸的生物合成。此外，我们证明了一个以前未被认识到的影响TCP对叶片衰老，茉莉酸已被提出的过程中是一个关键的调节器。我们提出，miR 319控制的TCP转录因子协调两个连续的过程中的叶片发育：叶片生长，他们负调控，和叶片衰老，他们积极调节。称为microRNA（miRNAs）的短单链RNA分子通过负控制它们通过序列互补性识别的靶信使RNA的稳定性和翻译来调节基因表达。在植物中，miRNA主要调节其他调节因子，即DNA结合转录因子。我们研究了拟南芥中由microRNA miR 319控制的5个TCP（TEOSINTE BRANCHED/CYCLOIDEA/PCF）转录因子调控的下游事件。先前已知miR 319调节的TCP对于限制叶子的生长是重要的。通过应用全基因组、生物化学和遗传学研究的组合，我们确定了新的TCP靶点，其中包括负责合成激素茉莉酸的酶。我们对miR 319活性增加的植物叶提取物的分析证实，生物合成基因的表达改变导致茉莉酸水平改变。这些植物也显示出改变的衰老行为，当植物用茉莉酸盐处理时，衰老行为再次变得更加正常。我们提出，miR 319调节的TCP因子因此协调叶发育和生理学的不同方面：生长，它们负调节，衰老，它们正调节。一种植物microRNA及其靶点可以调节叶片发育的早期和晚期：在早期，它们抑制生长，而在后期，它们促进衰老的开始。
Considerable progress has been made in identifying the targets of plant microRNAs, many of which regulate the stability or translation of mRNAs that encode transcription factors involved in development. In most cases, it is unknown, however, which immediate transcriptional targets mediate downstream effects of the microRNA-regulated transcription factors. We identified a new process controlled by the miR319-regulated clade of TCP (TEOSINTE BRANCHED/CYCLOIDEA/PCF) transcription factor genes. In contrast to other miRNA targets, several of which modulate hormone responses, TCPs control biosynthesis of the hormone jasmonic acid. Furthermore, we demonstrate a previously unrecognized effect of TCPs on leaf senescence, a process in which jasmonic acid has been proposed to be a critical regulator. We propose that miR319-controlled TCP transcription factors coordinate two sequential processes in leaf development: leaf growth, which they negatively regulate, and leaf senescence, which they positively regulate. Short, single-stranded RNA molecules called microRNAs (miRNAs) regulate gene expression by negatively controlling both the stability and translation of target messenger RNAs that they recognize through sequence complementarity. In plants, miRNAs mostly regulate other regulators, the DNA-binding transcription factors. We investigated the downstream events regulated by five TCP (TEOSINTE BRANCHED/CYCLOIDEA/PCF) transcription factors that are controlled by the microRNA miR319 in Arabidopsis thaliana. The miR319-regulated TCPs were previously known to be important for limiting the growth of leaves. By applying a combination of genome-wide, biochemical, and genetic studies, we identified new TCP targets that include enzymes responsible for the synthesis of the hormone jasmonic acid. Our analysis of leaf extracts from plants with increased activity of miR319 confirms that altered expression of the biosynthetic genes leads to changed jasmonic acid levels. These plants show also an altered senescence behavior that becomes more normal again when the plants are treated with jasmonate. We propose that the miR319-regulated TCP factors thus coordinate different aspects of leaf development and physiology: growth, which they negatively regulate, and aging, which they positively regulate. A plant microRNA and its targets turn out to regulate both early and late stages of leaf development: early on, they inhibit growth, while later on, they promote the onset of senescence.
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影响因子：
3.7
作者：
Fahlgren N;Howell MD;Kasschau KD;Chapman EJ;Sullivan CM;Cumbie JS;Givan SA;Law TF;Grant SR;Dangl JL;Carrington JC
通讯作者：
Carrington JC
影响因子：
64.8
作者：
Doebley, J;Stec, A;Hubbard, L
通讯作者：
Hubbard, L
影响因子：
5.1
作者：
Dugas, Diana V.;Bartel, Bonnie
通讯作者：
Bartel, Bonnie
影响因子：
7.4
作者：
Benedetti, CE;Costa, CL;Arruda, P
通讯作者：
Arruda, P
影响因子：
9.2
作者：
Fahlgren, Noah;Montgomery, Talowa A.;Carrington, James C.
通讯作者：
Carrington, James C.