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A more recent version of this article appeared on July 1, 2005
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Papers In Press, published online ahead of print May 6, 2005
J. Biol. Chem, 10.1074/jbc.M501784200
Submitted on February 16, 2005
Revised on May 5, 2005
Accepted on May 6, 2005

Transcription-induced chromatin remodeling at the C-Myc gene involves a local exchange of histone H2A.Z

Stephen D. Farris, Eric D. Rubio, James J. Moon, Wendy M. Gombert, Brad H. Nelson, and Anton Krumm

Radiation Oncology, University of Washington, Seattle, WA 98103

Corresponding Author: akrumm{at}u.washington.edu

The post-translational modification of histones and the incorporation of core histone variants play key roles in governing gene expression. Many eukaryotic genes regulate their expression by limiting the escape of RNA polymerase from promoter-proximal pause sites. Here we report that elongating RNA polymerase II complexes encounter distinct chromatin landscapes that are marked by methylation of lysine residues K4, K79 and K36 of histone H3. However, neither histone methylation nor acetylation directly regulates the release of elongation complexes stalled at promoter-proximal pause sites of the c-myc gene. In contrast, transcriptional activation is associated with local displacement of the histone variant H2A.Z within the transcribed region and incorporation of the major histone variant H2A. This result indicates that transcribing RNA pol II remodels chromatin in part through coincident displacement of H2A.Z-H2B dimers and incorporation of H2A-H2B dimers. In combination, these results suggest a new model in which the incorporation of H2A.Z into nucleosomes downregulates transcription; at the same time it may act as a cellular memory for transcriptionally poised gene domains.


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