Mobile 24 nt small RNAs direct transcriptional gene silencing in the root meristems of Arabidopsis thaliana - PubMed (original) (raw)
. 2011 Oct 11;21(19):1678-83.
doi: 10.1016/j.cub.2011.08.065. Epub 2011 Sep 29.
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- PMID: 21962713
- DOI: 10.1016/j.cub.2011.08.065
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Mobile 24 nt small RNAs direct transcriptional gene silencing in the root meristems of Arabidopsis thaliana
Charles W Melnyk et al. Curr Biol. 2011.
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Abstract
RNA silencing in flowering plants generates a signal that moves between cells and through the phloem [1, 2]. Nucleotide sequence specificity of the signal is conferred by 21, 22, and 24 nucleotide (nt) sRNAs that are generated by Dicer-like (DCL) proteins [3]. In the recipient cells these sRNAs bind to Argonaute (AGO) effectors of silencing and the 21 nt sRNAs mediate posttranscriptional regulation (PTGS) via mRNA cleavage [4] whereas the 24 nt sRNAs are associated with RNA-dependent DNA methylation (RdDM) [5] that may underlie transcriptional gene silencing (TGS). Intriguingly, genes involved in TGS are required for graft-transmissible gene silencing associated with PTGS [6]. However, some of the same genes were also required for spread of a PTGS silencing signal out of the veins of Arabidopsis [7], and grafting tests failed to demonstrate direct transmission of TGS signals [8-10]. It seemed likely, therefore, that mobile silencing is associated only with PTGS. To address this possibility, we grafted TGS-inducing wild-type Arabidopsis and a mutant that is compromised in 24 nt sRNA production onto a wild-type reporter line. The 21-24 nt sRNAs from the TGS construct were transmitted across a graft union but only the 24 nt sRNAs directed RdDM and TGS of a transgene promoter in meristematic cells. These data extend the significance of an RNA silencing signal to embrace epigenetics and transcriptional gene silencing and support the hypothesis that these signals transmit information to meristematic cells where they initiate persistent epigenetic changes that may influence growth, development, and heritable phenotypes.
Copyright © 2011 Elsevier Ltd. All rights reserved.
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