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.
© 2008 The Authors. Journal compilation © 2008 Blackwell Publishing Ltd.