Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Cell. 2010 Mar 5;140(5):666-77. doi: 10.1016/j.cell.2010.01.038.

Stc1: a critical link between RNAi and chromatin modification required for heterochromatin integrity.

Author information

  • 1Wellcome Trust Centre for Cell Biology and Institute of Cell Biology, School of Biological Sciences, The University of Edinburgh, Edinburgh EH9 3JR, Scotland, UK.

Abstract

In fission yeast, RNAi directs heterochromatin formation at centromeres, telomeres, and the mating type locus. Noncoding RNAs transcribed from repeat elements generate siRNAs that are incorporated into the Argonaute-containing RITS complex and direct it to nascent homologous transcripts. This leads to recruitment of the CLRC complex, including the histone methyltransferase Clr4, promoting H3K9 methylation and heterochromatin formation. A key question is what mediates the recruitment of Clr4/CLRC to transcript-bound RITS. We have identified a LIM domain protein, Stc1, that is required for centromeric heterochromatin integrity. Our analyses show that Stc1 is specifically required to establish H3K9 methylation via RNAi, and interacts both with the RNAi effector Ago1, and with the chromatin-modifying CLRC complex. Moreover, tethering Stc1 to a euchromatic locus is sufficient to induce silencing and heterochromatin formation independently of RNAi. We conclude that Stc1 associates with RITS on centromeric transcripts and recruits CLRC, thereby coupling RNAi to chromatin modification.

(c) 2010 Elsevier Inc. All rights reserved.

PMID:
20211136
[PubMed - indexed for MEDLINE]
PMCID:
PMC2875855
Free PMC Article

Images from this publication.See all images (13)Free text

Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure S1
Figure S2
Figure S3
Figure S4
Figure S5
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Icon for Elsevier Science Icon for PubMed Central Icon for Faculty of 1000
    Loading ...
    Write to the Help Desk