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Arabidopsis Argonaute10 Specifically Sequesters miR166/165 to Regulate Shoot Apical Meristem Development
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SUMMARY 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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Metadata
- Authors
- Zhu, H., Hu, F., Wang, R., Zhou, X., Sze, S.-H., Liou, L. W., Barefoot, A., Dickman, M., & Zhang, X.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2011-04
- Volume
- 145
- Issue
- 2
- Pages
- 242-256
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W1986352294
- Cited by
- 501
- References
- 44
- FWCI
- 36.69
- Type
- journal article
- Language
- en
- Open access
- bronze
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