This Article
Right arrow Full Text
Right arrow Full Text (PDF)
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 Pavelitz, T.
Right arrow Articles by Weiner, A. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pavelitz, T.
Right arrow Articles by Weiner, A. M.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, June 2008, p. 3573-3588, Vol. 28, No. 11
0270-7306/08/$08.00+0     doi:10.1128/MCB.00087-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Human U2 snRNA Genes Exhibit a Persistently Open Transcriptional State and Promoter Disassembly at Metaphase{triangledown}

Thomas Pavelitz, Arnold D. Bailey, Christopher P. Elco,{ddagger} and Alan M. Weiner*

Department of Biochemistry, School of Medicine, University of Washington, Seattle, Washington 98195-7350

Received 16 January 2008/ Returned for modification 26 February 2008/ Accepted 23 March 2008

In mammals, small multigene families generate spliceosomal U snRNAs that are nearly as abundant as rRNA. Using the tandemly repeated human U2 genes as a model, we show by footprinting with DNase I and permanganate that nearly all sequences between the enhancer-like distal sequence element and the initiation site are protected during interphase whereas the upstream half of the U2 snRNA coding region is exposed. We also show by chromatin immunoprecipitation that the SNAPc complex, which binds the TATA-like proximal sequence element, is removed at metaphase but remains bound under conditions that induce locus-specific metaphase fragility of the U2 genes, such as loss of CSB, BRCA1, or BRCA2 function, treatment with actinomycin D, or overexpression of the tetrameric p53 C terminus. We propose that the U2 snRNA promoter establishes a persistently open state to facilitate rapid reinitiation and perhaps also to bypass TFIIH-dependent promoter melting; this open state would then be disassembled to allow metaphase chromatin condensation.

* Corresponding author. Mailing address: University of Washington, Department of Biochemistry, Box 357350, School of Medicine, Seattle, WA 98195-7350. Phone: (206) 543-1768. Fax: (206) 685-9231. E-mail: amweiner{at}u.washington.edu

{triangledown} Published ahead of print on 31 March 2008.

{ddagger} Present address: Molecular Virology Program, Case Western Reserve University, 10900 Euclid Ave., Cleveland, OH 44106.

Molecular and Cellular Biology, June 2008, p. 3573-3588, Vol. 28, No. 11
0270-7306/08/$08.00+0     doi:10.1128/MCB.00087-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Egloff, S., Al-Rawaf, H., O'Reilly, D., Murphy, S. (2009). Chromatin Structure Is Implicated in "Late" Elongation Checkpoints on the U2 snRNA and {beta}-Actin Genes. Mol. Cell. Biol. 29: 4002-4013 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»