Polycomb preferentially targets stalled promoters of coding and noncoding transcripts
- Daniel Enderle1,4,
- Christian Beisel1,4,
- Michael B. Stadler2,
- Moritz Gerstung1,
- Prashanth Athri1,5 and
- Renato Paro1,3,6
- 1 Department of Biosystems Science and Engineering, ETH Zurich, CH-4058 Basel, Switzerland;
- 2 Friedrich Miescher Institute for Biomedical Research, CH-4058 Basel, Switzerland;
- 3 Faculty of Science, University of Basel, CH-4056 Basel, Switzerland
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↵4 These authors contributed equally to this work.
Abstract
The Polycomb group (PcG) and Trithorax group (TrxG) of proteins are required for stable and heritable maintenance of repressed and active gene expression states. Their antagonistic function on gene control, repression for PcG and activity for TrxG, is mediated by binding to chromatin and subsequent epigenetic modification of target loci. Despite our broad knowledge about composition and enzymatic activities of the protein complexes involved, our understanding still lacks important mechanistic detail and a comprehensive view on target genes. In this study we use an extensive data set of ChIP-seq, RNA-seq, and genome-wide detection of transcription start sites (TSSs) to identify and analyze thousands of binding sites for the PcG proteins and Trithorax from a Drosophila S2 cell line. In addition of finding a preference for stalled promoter regions of annotated genes, we uncover many intergenic PcG binding sites coinciding with nonannotated TSSs. Interestingly, this set includes previously unknown promoters for primary transcripts of microRNA genes, thereby expanding the scope of Polycomb control to noncoding RNAs essential for development, apoptosis, and growth.
Footnotes
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↵6 Corresponding author.
E-mail renato.paro{at}bsse.ethz.ch; fax 41-61-387-39-96.
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[Supplemental material is available for this article. The sequence data from this study have been submitted to the NCBI Gene Expression Omnibus (http://www.ncbi.nlm.nih.gov/geo) under accession no. GSE24521.]
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Article published online before print. Article, supplemental material, and publication date are at http://www.genome.org/cgi/doi/10.1101/gr.114348.110.
- Received October 8, 2010.
- Accepted November 22, 2010.
- Copyright © 2011 by Cold Spring Harbor Laboratory Press
Freely available online through the Genome Research Open Access option.
