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MicroRNA Directs mRNA Cleavage of the Transcription Factor NAC1 to Downregulate Auxin Signals for Arabidopsis Lateral Root Development

机译:MicroRNA指导转录因子NAC1的mRNA切割,以下调拟南芥侧根发育的生长素信号。

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摘要

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 wild-type 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 3′ 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.
机译:尽管已经显示了几种植物微RNA(miRNA)在植物发育中起作用,但是尚未有任何表型与任何植物miRNA的表达减少或丧失相关。拟南芥拟南芥miR164靶向5个NAM / ATAF / CUC(NAC)域编码mRNA,包括NAC1,后者可为侧根出苗转导生长素信号。在这里,我们显示miR164指导内源性和转基因NAC1 mRNA的裂解,产生3'特异性片段。 NAC1突变阻断了与miR164碱基配对的切割,阻断了切割。与野生型植物相比,拟南芥mir164a和mir164b突变体植物表达的miR164更少,NAC1 mRNA则更多,并且产生更多的侧根。这些突变表型可以通过适当的MIR164a和MIR164b基因组序列的表达来补充。相比之下,miR164在野生型植物中的诱导表达导致NAC1 mRNA水平降低和侧根出现减少。 NAC1 mRNA 3'片段的增加反映了生长素诱导miR164的生长,这在生长素不敏感的生长素抗性突变体生长素抗性1(axr1-12),axr2-1和转运抑制剂response1中未观察到。而且,NAC1 mRNA的抗切割形式不受生长素处理的影响。我们的结果表明,miR164的生长素诱导提供了一种稳态机制,以清除NAC1 mRNA来下调生长素信号。

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