Plants have the ability to regenerate whole plant body parts, including shoots and roots, in vitro from callus derived from a variety of tissues. However, the underlying mechanisms for this de novo organogenesis, which is based on the totipotency of callus cells, are poorly understood. Here, we report that a microRNA (miRNA)-mediated posttranscriptional regulation plays an important role in de novo shoot regeneration. We found that mutations in HUA ENHANCER 1 (HEN1), a gene encoding a small RNA methyltransferase, cause cytokinin-related defects in de novo shoot regeneration. A hen1 mutation caused a large reduction in the miRNA319 (miR319) level and a subsequent increase in its known target (TCP3 and TCP4) transcript levels. TCP transcription factors redundantly inhibited shoot regeneration and directly activated the expression of a negative regulator of cytokinin response ARABIDOPSIS THALIANA RESPONSE REGULATOR 16 (ARR16). A tcp4 mutation at least partly rescued the shoot-regeneration defect and derepression of ARR16 in hen1. These findings demonstrate that the miR319-TCP3/4-ARR16 axis controls de novo shoot regeneration by modulating cytokinin responses.

中文翻译：

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拟南芥中由HEN1和TCP3 / 4控制的新芽再生。

植物具有在体外从衍生自多种组织的愈伤组织中再生整个植物身体部分（包括芽和根）的能力​​。然而，基于愈伤组织细胞全能性的这种从头器官发生的基本机制了解甚少。在这里，我们报告说，microRNA（miRNA）介导的转录后调控在从头芽再生中起重要作用。我们发现，HUA ENHANCER 1（HEN1）（一种编码小RNA甲基转移酶的基因）中的突变在从头芽再生中引起细胞分裂素相关的缺陷。甲HEN1突变引起在miRNA319（miR319）大的减速级，并在其已知的靶（一个随后增加TCP3和TCP4）的成绩单水平。TCP转录因子多余地抑制了芽的再生，并直接激活了细胞分裂素反应的负调节剂阿拉伯海藻反应调节剂16（ARR16）的表达。一个TCP4突变至少部分获救的芽再生缺陷和去阻遏ARR16在HEN1。这些发现表明，miR319-TCP3 / 4-ARR16轴通过调节细胞分裂素应答来控制新芽的再生。