miR393 is required for production of proper auxin signalling outputs.

miR393 is required for production of proper auxin signalling outputs.
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DOI:
10.1371/journal.pone.0095972
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发表时间:
2014
期刊:
影响因子:
3.7
通讯作者:
Vazquez F
Vazquez F
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Windels D;Bielewicz D;Ebneter M;Jarmolowski A;Szweykowska-Kulinska Z;Vazquez F

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甜菜碱对植物的生长和发育至关重要。生长素信号传导主要依赖于TIR 1/AFB 2生长素受体(TAAR)进化枝的四个部分冗余的F-box蛋白来触发AUX/IAA转录抑制因子的降解。生长素信号是一个平衡的系统,涉及复杂的反馈调节。TAAR基因的miR 393调节对于不同的发育程序和对环境的响应是重要的。然而,到目前为止,这两个MIR 393基因的拟南芥叶片发育和生长素信号稳态的意义的相关性还没有得到评估。首先,我们对mir 393 a-1和mir 393 b-1突变体以及mir 393 ab双突变体的分析表明,这两个基因对叶片发育只有部分冗余功能。典型的生长素诱导的报告基因的表达分析表明,miR 393的损失导致生长素信号的几个意想不到的变化。在mir 393 ab突变体中,DR 5 pro:GUS的表达降低,主要的AUX/IAA生长素响应基因的表达略有增加,AXR 3-NT:GUS报告蛋白的降解延迟。使用合成的生长素和生长素拮抗剂的另外的分析表明,miR 393缺陷突变体具有更高水平的内源AUX/IAA蛋白,这反过来又产生降解竞争。我们提出,AUX/IAA基因的表达和AUX/IAA蛋白的积累中的反直觉的变化被解释为AUX/IAA基因的内在性质,其由它们产生的AUX/IAA蛋白反馈调节。总之,我们的实验提供了一个额外的亮点生长素信号稳态的复杂性,并显示,miR 393是这种稳态的重要组成部分。
Auxins are crucial for plant growth and development. Auxin signalling primarily depends on four partially redundant F-box proteins of the TIR1/AFB2 Auxin Receptor (TAAR) clade to trigger the degradation of AUX/IAA transcriptional repressors. Auxin signalling is a balanced system which involves complex feedback regulations. miR393 regulation of TAAR genes is important for different developmental programs and for responses to environment. However, so far, the relevance of the two MIR393 genes for Arabidopsis leaf development and their significance for auxin signalling homeostasis have not been evaluated. First, our analyses of mir393a-1 and mir393b-1 mutants and of mir393ab double mutant show that the two genes have only partially redundant functions for leaf development. Expression analyses of typical auxin-induced reporter genes have shown that the loss of miR393 lead to several unanticipated changes in auxin signalling. The expression of DR5pro:GUS is decreased, the expression of primary AUX/IAA auxin-responsive genes is slightly increased and the degradation of the AXR3-NT:GUS reporter protein is delayed in mir393ab mutants. Additional analyses using synthetic auxin and auxin antagonists indicated that miR393 deficient mutants have higher levels of endogenous AUX/IAA proteins, which in turn create a competition for degradation. We propose that the counter-intuitive changes in the expression of AUX/IAA genes and in the accumulation of AUX/IAA proteins are explained by the intrinsic nature of AUX/IAA genes which are feedback regulated by the AUX/IAA proteins which they produce. Altogether our experiments provide an additional highlight of the complexity of auxin signaling homeostasis and show that miR393 is an important component of this homeostasis.
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