Format

Send to

Choose Destination
See comment in PubMed Commons below
Cell. 2011 Apr 15;145(2):242-56. doi: 10.1016/j.cell.2011.03.024.

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

Author information

1
Department of Biochemistry and Biophysics, Texas A&M University, College Station, TX 77843, USA.

Abstract

The shoot apical meristem (SAM) comprises a group of undifferentiated cells that divide to maintain the plant meristem and also give rise to all shoot organs. SAM fate is specified by class III HOMEODOMAIN-LEUCINE ZIPPER (HD-ZIP III) transcription factors, which are targets of miR166/165. In Arabidopsis, AGO10 is a critical regulator of SAM maintenance, and here we demonstrate that AGO10 specifically interacts with miR166/165. The association is determined by a distinct structure of the miR166/165 duplex. Deficient loading of miR166 into AGO10 results in a defective SAM. Notably, the miRNA-binding ability of AGO10, but not its catalytic activity, is required for SAM development, and AGO10 has a higher binding affinity for miR166 than does AGO1, a principal contributor to miRNA-mediated silencing. 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 III gene expression.

Comment in

PMID:
21496644
PMCID:
PMC4124879
DOI:
10.1016/j.cell.2011.03.024
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center