The shoot apical meristem (SAM) of angiosperms comprises a group of undifferentiated cells which divide to maintain the meristem and also give rise to all the above‐ground structures of the plant. Previous studies revealed that the Arabidopsis ARGONAUTE10 [AGO10, also called PINHEAD (PNH) or ZWILLE (ZLL)] gene is one of the critical SAM regulators, but the mechanism by which AGO10 modulates the SAM is unknown. In the present study we show that AGO10 genetically represses microRNA165/166 (miR165/166) for SAM maintenance as well as establishment of leaf adaxial–abaxial polarity. Levels of miR165/166 in leaves and embryonic SAMs of pnh/zll/ago10 mutants are abnormally elevated, leading to a reduction in the quantity of homeodomain‐leucine zipper (HD‐ZIP) III gene transcripts, the targets of miR165/166. This reduction is the primary cause of pnh/zll SAM and leaf defects, because the aberrant pnh/zll phenotypes were partially rescued by either increasing levels of HD‐ZIP III transcripts or decreasing levels of miR165/166 in the SAM and leaf. Furthermore, plants with an abnormal apex were more frequent among pnh/zll rdr6 and pnh/zll ago7 double mutants and increased levels of miR165/166 were detected in rdr6 apices. These results indicate that AGO10 and RDR6/AGO7 may act in parallel in modulating accumulation of miR165/166 for normal plant development.

中文翻译：

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ARGONAUTE10基因通过抑制拟南芥中的miR165 / 166来调节茎尖分生组织的维持和叶片极性的建立

被子植物的茎尖分生组织（SAM）包括一组未分化的细胞，这些细胞分裂以维持分生组织，并产生植物的所有地上结构。以前的研究显示，拟南芥ARGONAUTE10 [ AGO10，也称为针头（PNH）或ZWILLE（ZLL）]基因是临界SAM调节器中的一个，但通过该机构AGO10调制SAM是未知的。在本研究中，我们表明AGO10遗传抑制SAM维持以及建立叶片前后轴极性的microRNA165 / 166（miR165 / 166）。叶片和胚SAMs中miR165 / 166的水平。PNH / ZLL / ago10突变体异常升高，从而导致在同源结构域-亮氨酸拉链（HD-ZIP）III基因转录物，miR165 / 166的目标的量的减少。这种减少是的主要原因PNH / ZLL SAM和叶的缺陷，这是因为异常PNH / ZLL表型由HD-ZIP III转录物或在SAM和叶miR165 / 166的水平降低的或者增加水平部分获救。此外，在pnh / zll rdr6和pnh / zll ago7中，具有顶点异常的植物更为常见。在rdr6末端检测到双突变体和miR165 / 166水平升高。这些结果表明，AGO10和RDR6 / AGO7可能在正常植物发育的miR165 / 166积累调节中并行发挥作用。