Tight protein–DNA interactions favor gene silencing
- Marion Dubarry1,2,3,
- Isabelle Loïodice1,2,3,
- Chunlong L. Chen4,
- Claude Thermes4 and
- Angela Taddei1,2,3,5
- 1Institut Curie, Paris, F-75248 France;
- 2CNRS, UMR 218, Paris, F-75248 France;
- 3UPMC, Paris, F-75248 France;
- 4Centre de Génétique Moléculaire, CNRS, UPR3404, Gif-sur-Yvette F-91198, France
Abstract
The heterochromatin-like structure formed by the yeast silent information regulator complex (SIR) represses transcription at the silent mating type loci and telomeres. Here, we report that tight protein–DNA complexes induce ectopic recruitment of the SIR complex, promoting gene silencing and changes in subnuclear localization when cis-acting elements are nearby. Importantly, lack of the replication fork-associated helicase Rrm3 enhances this induced gene repression. Additionally, Sir3 and Sir4 are enriched genome-wide at natural replication pause sites, including tRNA genes. Consistently, inserting a tRNA gene promotes SIR-mediated silencing of a nearby gene. These results reveal that replication stress arising from tight DNA–protein interactions favors heterochromatin formation.
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Footnotes
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↵5 Corresponding author.
E-mail angela.taddei{at}curie.fr.
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Supplemental material is available for this article.
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Article is online at http://www.genesdev.org/cgi/doi/10.1101/gad.611011.
- Received September 28, 2010.
- Accepted May 23, 2011.
- Copyright © 2011 by Cold Spring Harbor Laboratory Press