Skip Navigation



Nucleic Acids Research Advance Access published online on August 1, 2008
Nucleic Acids Research, doi:10.1093/nar/gkn484
This Article
Right arrow Full Text Freely available
Right arrow Print PDF (2373K) Freely available
Right arrow Screen PDF (1851K) Freely available
Right arrow Supplementary Data
Right arrowOA All Versions of this Article:
36/15/5093    most recent
gkn484v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Stefanovsky, V. Y.
Right arrow Articles by Moss, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Stefanovsky, V. Y.
Right arrow Articles by Moss, T.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gene regulation, Chromatin and Epigenetics

The splice variants of UBF differentially regulate RNA polymerase I transcription elongation in response to ERK phosphorylation

Victor Y. Stefanovsky and Tom Moss*

Cancer Research Centre and Department of Medical Biology of Laval University, Centre de Recherche de l’Hôtel-Dieu de Québec, 9 rue McMahon, G1R 3S3 Québec, QC, Canada

*To whom correspondence should be addressed. Tel: +418 691 5281; Fax: +418 691 5439; Email: tom.moss{at}crhdq.ulaval.ca

Received May 29, 2008. Revised July 11, 2008. Accepted July 12, 2008.

The mammalian architectural HMGB-Box transcription factor UBF is ubiquitously expressed in two variant forms as the result of a differential splicing event, that in the UBF2 deletes 37 amino acid from the second of six HMGB-boxes. Several attempts to define a function for this shorter UBF2 protein have been less than satisfactory. However, since all mammals appear to display similar levels of the longer and shorter UBF variants, it is unlikely that UBF2 is simply nonfunctional. Previously we showed that phosphorylation of UBF by the MAP-kinase ERK regulates chromatin folding and transcription elongation, explaining the rapid response of the ribosomal RNA genes to growth factors. Here we have investigated the roles the UBF variants play in the response of these genes to ERK activity. We demonstrate that the variant HMGB-box 2 of UBF2 has lost the ability to bind bent DNA and hence to induce chromatin folding. As a result it is significantly less effective than UBF1 at arresting RNAPI elongation but at the same time is more responsive to ERK phosphorylation. Thus, UBF2 functionally simulates a hemi-phosphorylated UBF whose expression may provide a means by which to tune the response of the ribosomal RNA genes to growth factor stimulation.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Nucleic Acids ResHome page
T. A. Gangelhoff, P. S. Mungalachetty, J. C. Nix, and M. E. A. Churchill
Structural analysis and DNA binding of the HMG domains of the human mitochondrial transcription factor A
Nucleic Acids Res., June 1, 2009; 37(10): 3153 - 3164.
[Abstract] [Full Text] [PDF]

Home page
 JCBHome page
E. Sanij, G. Poortinga, K. Sharkey, S. Hung, T. P. Holloway, J. Quin, E. Robb, L. H. Wong, W. G. Thomas, V. Stefanovsky, et al.
UBF levels determine the number of active ribosomal RNA genes in mammals
J. Cell Biol., December 29, 2008; 183(7): 1259 - 1274.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.