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当前位置: 博奥晶典 > 最新动态 > The Plant Journal文章:拟南芥再生需要miRNA介导的生长素反

The Plant Journal文章:拟南芥再生需要miRNA介导的生长素反

博奥晶典

2012/04/20 14:03

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 The Plant Journal文章:拟南芥再生需要miRNA介导的生长素反应活性

  miRNA对基因表达具有重要调控作用,广泛参与多种发育调控过程。首先鉴定出了一组在拟南芥愈伤组织中全能细胞(C1)和非全能(C2)细胞中具有差异表达的miRNA,其中一些miRNA在愈伤形成或芽再生过程中也有变化。MiR160a是一个在芽诱导培养基(SIM)培养10天后下调表达,在C1细胞其表达丰度较C2细胞也具有明显降低。MiR160过表达妨碍拟南芥体外培养细胞芽再生过程。转基因导入的miR106拮抗体ARF10可以高水平提高芽再生能力,转基因细胞系同时显示芽分生组织特异性基因如CLAVATA3, CUP - SHAPEDCOTYLEDON 1 /2, WUSCHEL的高水平表达。ARF10的表达主要集中在芽和叶的生长位点,在芽再生的早期阶段野生型ARF10表达量低于mARF10转基因细胞,这与miR160表达模式相反。因此,miR160和ARF10都参与拟南芥体外培养的芽再生过程调控。

上述研究中,晶芯miRNA芯片服务博奥生物有限公司完成。
原文摘要:
Proper regeneration from in vitro cultured Arabidopsis thaliana requires the miRNA directed action of an auxin response factor
MicroRNAs (miRNAs) are important for the regulation of gene expression, and are involved in many developmental processes. A set of miRNAs which were differentially expressed between cells of totipotent (C1) and non-totipotent (C2) Arabidopsis thaliana calli was identified, some of which were affected during callus formation or shoot regeneration. One of those down-regulated after 10 d incubation in shoot induction medium (SIM) was MIR160a, for which transcript abundance was lower in C1 than in C2. Over-expression of MIR160 compromised shoot regeneration from in vitro cultured A. thaliana cells, while the transgenic expression of a miR160-resistant form of ARF10 was associated with a high level of shoot regeneration. The latter transgenic line also showed an elevated expression level of shoot meristem-specific genes CLAVATA3, CUP-SHAPEDCOTYLEDON 1 and 2, and WUSCHEL. ARF10 expression was concentrated at the initiation sites of shoots or leaves, while during the early phase of shoot regeneration, the accumulation of the ARF10 message was lower in the wild type than in the mARF10 transgenics, in contrast to the pattern of miR160 expression. Thus, miR160 and ARF10 both appear to be components of the regulation of shoot regeneration in vitro.
原文出处:http://onlinelibrary.wiley.com/doi/10.1111/j.1365-313X.2012.04944.x/abstract

 

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