Arabidopsis Argonaute10 specifically sequesters miR166/165 to regulate shoot apical meristem development.

Arabidopsis Argonaute10 specifically sequesters miR166/165 to regulate shoot apical meristem development.
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DOI:
10.1016/j.cell.2011.03.024
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发表时间:
2011-04-15
期刊:
影响因子:
64.5
通讯作者:
Zhang X
Zhang X
中科院分区:
生物学1区
文献类型:
--
作者:
Zhu H;Hu F;Wang R;Zhou X;Sze SH;Liou LW;Barefoot A;Dickman M;Zhang X

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顶端分生组织(SAM)由一组未分化的细胞组成,这些细胞分裂以维持分生组织,也形成所有植物的茎器官。SAM命运由同源结构域-亮氨酸拉链(HD-ZIP)转录因子决定,这些转录因子是miR166/165的靶标。在拟南芥中,AGO10是SAM维持的关键调节因子,但其调节机制尚不清楚。在这里,我们证明AGO10专门招募miR166/165。AGO10-miR166/165的关联由miR166/165双链的不同结构决定。将miR166加载到AGO10中的不足导致SAM有缺陷。AGO10与miR166的结合亲和力高于Ago1,Ago1是miRNA靶标的主要抑制子。值得注意的是,SAM的开发需要AGO10与miR166/165的结合能力,而不是其催化活性。我们认为AGO10作为miR166/165的诱饵来维持SAM,阻止它们掺入Ago1复合体,从而抑制HD-ZIP基因的表达。
The shoot apical meristem (SAM) comprises a group of undifferentiated cells that divide to maintain the meristem and also give rise to all plant shoot organs. SAM fate is specified by HOMEODOMAIN-LEUCINE ZIPPER (HD-ZIP) transcription factors, which are targets of miR166/165. In Arabidopsis, AGO10 is a critical regulator of SAM maintenance, but the mechanism of regulation remains unknown. Here we demonstrate that AGO10 specifically recruits miR166/165. The AGO10-miR166/165 association is determined by the distinct structure of the miR166/165 duplex. Deficient loading of miR166 into AGO10 results in a defective SAM. AGO10 has a higher binding affinity for miR166 than does AGO1, a master repressor for miRNA targets. Notably, the miR166/165-binding ability of AGO10, but not its catalytic activity, is required for SAM development. We propose that AGO10 functions as a decoy for miR166/165 to maintain the SAM, preventing their incorporation into AGO1 complexes and the subsequent repression of HD-ZIP gene expression.
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