Skip Navigation



Nucleic Acids Research Advance Access published online on December 2, 2008
Nucleic Acids Research, doi:10.1093/nar/gkn955
This Article
Right arrow Full Text Freely available
Right arrow Print PDF (3110K) Freely available
Right arrow Screen PDF (458K) Freely available
Right arrowOA All Versions of this Article:
37/2/431    most recent
gkn955v1
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 Green, L. M.
Right arrow Articles by Roberts, S. G. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Green, L. M.
Right arrow Articles by Roberts, S. G. E.
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

Dynamic interaction between WT1 and BASP1 in transcriptional regulation during differentiation

Laura M. Green, Kate J. Wagner, Hayley A. Campbell, Kelly Addison and Stefan G. E. Roberts*

Faculty of Life Sciences, The Michael Smith Building University of Manchester Oxford Road, Manchester M13 9PT, UK

*To whom correspondence should be addressed. Tel: +44 0161 275 5758; Fax: +44 0161 275 5082; Email: stefan.roberts{at}manchester.ac.uk

Received September 30, 2008. Revised November 10, 2008. Accepted November 10, 2008.

The Wilms’ tumour suppressor protein WT1 plays a central role in the development of the kidney and also other organs. WT1 can act as a transcription factor with highly context-specific activator and repressor functions. We previously identified Brain Acid Soluble Protein 1 (BASP1) as a transcriptional cosuppressor that can block the transcriptional activation function of WT1. WT1 and BASP1 are co-expressed during nephrogenesis and both proteins ultimately become restricted to the podocyte cells of the adult kidney. Here, we have analysed the WT1/BASP1 complex in a podocyte precursor cell line that can be induced to differentiate. Chromatin immunoprecipitation revealed that WT1 and BASP1 occupy the promoters of the Bak, c-myc and podocalyxin genes in podocyte precursor cells. During differentiation-dependent upregulation of podocalyxin expression BASP1 occupancy of the podocalyxin promoter is reduced compared to that of WT1. In contrast, the repressive WT1/BASP1 occupancy of the c-myc and Bak promoters is maintained and these genes are downregulated during the differentiation process. We provide evidence that the regulation of BASP1 promoter occupancy involves the sumoylation of BASP1. Our results reveal a dynamic cooperation between WT1 and BASP1 in the regulation of gene expression during differentiation.


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
 Proc. Natl. Acad. Sci. USAHome page
M. Hartl, A. Nist, M. I. Khan, T. Valovka, and K. Bister
Inhibition of Myc-induced cell transformation by brain acid-soluble protein 1 (BASP1)
PNAS, April 7, 2009; 106(14): 5604 - 5609.
[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.