This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental material
Right arrow Supplemental material
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Parra, M. A.
Right arrow Articles by Wyrick, J. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Parra, M. A.
Right arrow Articles by Wyrick, J. J.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, November 2007, p. 7641-7648, Vol. 27, No. 21
0270-7306/07/$08.00+0     doi:10.1128/MCB.00742-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Regulation of Gene Transcription by the Histone H2A N-Terminal Domain{triangledown} ,{dagger}

Michael A. Parra and John J. Wyrick*

School of Molecular Biosciences, Washington State University, Pullman, Washington 99164-4660

Received 27 April 2007/ Returned for modification 19 June 2007/ Accepted 13 August 2007

Histone N-terminal domains play critical roles in regulating chromatin structure and gene transcription. Relatively little is known, however, about the role of the histone H2A N-terminal domain in transcription regulation. We have used DNA microarrays to characterize the changes in genome-wide expression caused by mutations in the N-terminal domain of histone H2A. Our results indicate that the N-terminal domain of histone H2A functions primarily to repress the transcription of a large subset of the Saccharomyces cerevisiae genome and that most of the H2A-repressed genes are also repressed by the histone H2B N-terminal domain. Using the histone H2A microarray data, we selected three reporter genes (BNA1, BNA2, and GCY1), which we subsequently used to map regions in the H2A N-terminal domain responsible for this transcriptional repression. These studies revealed that a small subdomain in the H2A N-terminal tail, comprised of residues 16 to 20, is required for the transcriptional repression of these reporter genes. Deletion of either the entire histone H2A N-terminal domain or just this small subdomain imparts sensitivity to UV irradiation. Finally, we show that two residues in this H2A subdomain, serine-17 and arginine-18, are specifically required for the transcriptional repression of the BNA2 reporter gene.


* Corresponding author. Mailing address: School of Molecular Biosciences, Washington State University, Fulmer Hall 675, Pullman, WA 99164-4660. Phone: (509) 335-8785. Fax: (509) 335-9688. E-mail: jwyrick{at}wsu.edu

{triangledown} Published ahead of print on 27 August 2007.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.


Molecular and Cellular Biology, November 2007, p. 7641-7648, Vol. 27, No. 21
0270-7306/07/$08.00+0     doi:10.1128/MCB.00742-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.