李霞研究组Plant Cell发现小分子RNA在固氮方面的作用

　　

　大豆根瘤共生固氮是一个非常重要的科学问题，也是一个关乎大豆产量和品质的重要农艺性状。最适的结瘤数量是决定最佳固氮效率的关键因子。已有结果发现结瘤因子诱导的信号转导途径和大豆超结瘤的自主调控途径（AON：Autoregulation）控制最适结瘤数量。但是两个途径互作的分子机制还不清楚。

　　中国科学院遗传与发育生物学研究所农业资源研究中心李霞课题组研究证明，在没有根瘤菌的情况下，大豆转录抑制子Nodule Number Control 1（GmNNC1）与结瘤调控因子ENOD40基因的启动子结合，抑制其表达；当根瘤菌侵染大豆根系时，诱导microRNA172c（miR172c）表达，miR172c进而通过剪切GmNNC1 mRNA减少GmNNC1的蛋白量，去除了转录抑制子GmNNC1对ENOD40的抑制；使得EOND40进一步激活了结瘤因子诱导的信号转导途径，从而启动了根瘤的发生发育。

    同时证明了抑制大豆超结瘤的自主调控途径（AON：Autoregulation）可通过Shoot-derived inhibitor如细胞分裂素来抑制miR172c的表达，从而避免大豆过度结瘤。

　　该研究揭示了豆科植物根瘤发育及共生固氮的表观遗传学调控机制，也为解析豆科植物根系结瘤途径与根瘤自调控信号途径互作维持最适根瘤数量和固氮效率的遗传机理提供了证据。

　　该研究成果于2014年12月31日在线发表于《植物细胞》（The Plant Cell）上。李霞课题组的副研究员王幼宁、博士研究生王利祥和邹艳敏为该文章的共同第一作者。该项目得到了国家自然科学基金委、农业部、植物细胞和染色体工程国家重点实验室与中国科学院“****”以及“青年创新促进会”的资助。

miR172c调控大豆根系结瘤过程的工作模型

原文摘要：

Soybean miR172c Targets the Repressive AP2 Transcription Factor NNC1 to Activate ENOD40 Expression and Regulate Nodule Initiation

MicroRNAs are noncoding RNAs that act as master regulators to modulate various biological processes by posttranscriptionally repressing their target genes. Repression of their target mRNA(s) can modulate signaling cascades and subsequent cellular events. Recently, a role for miR172 in soybean (Glycine max) nodulation has been described; however, the molecular mechanism through which miR172 acts to regulate nodulation has yet to be explored. Here, we demonstrate that soybean miR172c modulates both rhizobium infection and nodule organogenesis. miR172c was induced in soybean roots inoculated with either compatible Bradyrhizobium japonicum or lipooligosaccharide Nod factor and was highly upregulated during nodule development. Reduced activity and overexpression of miR172c caused dramatic changes in nodule initiation and nodule number. We show that soybean miR172c regulates nodule formation by repressing its target gene, Nodule Number Control1, which encodes a protein that directly targets the promoter of the early nodulin gene, ENOD40. Interestingly, transcriptional levels of miR172c were regulated by both Nod Factor Receptor1α/5α-mediated activation and by autoregulation of nodulation-mediated inhibition. Thus, we established a direct link between miR172c and the Nod factor signaling pathway in addition to adding a new layer to the precise nodulation regulation mechanism of soybean.