MicroRNA directs mRNA cleavage of the transcription factor NAC1 to downregulate auxin signals for Arabidopsis lateral root development
MicroRNA directs mRNA cleavage of the transcription factor NAC1 to downregulate auxin signals for Arabidopsis lateral root development
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DOI：
10.1105/tpc.105.030841
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发表时间：
2005-05-01
期刊：
影响因子：
11.6
通讯作者：
Chua, NH
中科院分区：
文献类型：
--
作者：
Guo, HS;Xie, Q;Chua, NH
虽然几种植物microRNA（miRNAs）已被证明在植物发育中起作用，但还没有表型与任何植物miRNAs表达的减少或丧失相关。拟南芥miR 164被预测靶向五个NAM/ATAF/CUC（NAC）结构域编码mRNA，包括NAC 1，其转导生长素信号用于侧根出现。在这里，我们发现miR 164引导内源性和转基因NAC 1 mRNA的切割，产生3 '特异性片段。裂解被破坏与miR 164的碱基配对的NAC 1突变阻断。与野生型植株相比，拟南芥mir 164 a和mir 164 b突变体植株miR 164表达量减少，NAC 1 mRNA表达量增加，侧根产生量增加。这些突变表型可以通过表达适当的MIR 164 a和MIR 164 b基因组序列来补充。相比之下，野生型植物中miR 164的诱导型表达导致NAC 1 mRNA水平降低和侧根出现减少。miR 164的生长素诱导通过NAC 1 mRNA 39片段的增加来反映，这在生长素不敏感突变体生长素抗性1（axr 1 -12）、axr 2 -1和运输抑制剂响应1中未观察到。此外，NAC 1 mRNA的抗切割形式不受生长素处理的影响。我们的研究结果表明，生长素诱导miR 164提供了一种稳态机制，以清除NAC 1 mRNA下调生长素信号。
Although several plant microRNAs (miRNAs) have been shown to play a role in plant development, no phenotype has yet been associated with a reduction or loss of expression of any plant miRNA. Arabidopsis thaliana miR164 was predicted to target five NAM/ATAF/CUC (NAC) domain-encoding mRNAs, including NAC1, which transduces auxin signals for lateral root emergence. Here, we show that miR164 guides the cleavage of endogenous and transgenic NAC1 mRNA, producing 3'-specific fragments. Cleavage was blocked by NAC1 mutations that disrupt base pairing with miR164. Compared with wildtype plants, Arabidopsis mir164a and mir164b mutant plants expressed less miR164 and more NAC1 mRNA and produced more lateral roots. These mutant phenotypes can be complemented by expression of the appropriate MIR164a and MIR164b genomic sequences. By contrast, inducible expression of miR164 in wild-type plants led to decreased NAC1 mRNA levels and reduced lateral root emergence. Auxin induction of miR164 was mirrored by an increase in the NAC1 mRNA 39 fragment, which was not observed in the auxin-insensitive mutants auxin resistant1 (axr1-12), axr2-1, and transport inhibitor response1. Moreover, the cleavage-resistant form of NAC1 mRNA was unaffected by auxin treatment. Our results indicate that auxin induction of miR164 provides a homeostatic mechanism to clear NAC1 mRNA to downregulate auxin signals.