MCB
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Oki, M.
Right arrow Articles by Kamakaka, R. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Oki, M.
Right arrow Articles by Kamakaka, R. T.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, March 2004, p. 1956-1967, Vol. 24, No. 5
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.5.1956-1967.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Barrier Proteins Remodel and Modify Chromatin To Restrict Silenced Domains{dagger}

Masaya Oki,1 Lourdes Valenzuela,1 Tomoko Chiba,2 Takashi Ito,2 and Rohinton T. Kamakaka1*

Unit on Chromatin and Transcription, National Institute of Child Health and Human Development, Bethesda, Maryland 20892,1 Division of Genome Biology, Cancer Research Institute, Kanazawa University, Kanazawa 920-0934, Japan2

Received 8 October 2003/ Returned for modification 17 November 2003/ Accepted 9 December 2003

Transcriptionally active and inactive domains are frequently found adjacent to one another in the eukaryotic nucleus. To better understand the underlying mechanisms by which domains maintain opposing transcription patterns, we performed a systematic genomewide screen for proteins that may block the spread of silencing in yeast. This analysis identified numerous proteins with efficient silencing blocking activities, and some of these have previously been shown to be involved in chromatin dynamics. We isolated subunits of Swi/Snf, mediator, and TFIID, as well as subunits of the Sas-I, SAGA, NuA3, NuA4, Spt10p, Rad6p, and Dot1p complexes, as barrier proteins. We demonstrate that histone acetylation and chromatin remodeling occurred at the barrier and correlated with a block to the spread of silencing. Our data suggest that multiple overlapping mechanisms were involved in delimiting silenced and active domains in vivo.

* Corresponding author. Mailing address: NIH, UCT/NICHD, Bldg. 18T, Rm. 106, 18 Library Dr., Bethesda, MD 20892. Phone: (301) 402-8317. Fax: (301) 402-1323. E-mail: rohinton{at}helix.nih.gov.

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

Molecular and Cellular Biology, March 2004, p. 1956-1967, Vol. 24, No. 5
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.5.1956-1967.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2004 by the American Society for Microbiology. All rights reserved.