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Nucleic Acids Research Advance Access originally published online on June 26, 2009
Nucleic Acids Research 2009 37(16):5378-5389; doi:10.1093/nar/gkp544
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Nucleic Acids Research, 2009, Vol. 37, No. 16 5378-5389
© 2009 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.

Molecular Biology

JunB mediates enhancer/promoter activity of COL1A2 following TGF-β induction

Markella Ponticos1, Clare Harvey2, Tetsuro Ikeda2, David Abraham1 and George Bou-Gharios2,*

1Department of Medicine, Centre for Rheumatology, University College London (Royal Free Campus) Rowland Hill Street, London NW3 2PF and 2Kennedy Institute of Rheumatology, Imperial College London, 65 Aspenlea Road, London W6 8LH, UK

*To whom correspondence should be addressed. Tel: 02083834413; Fax: 02083834499; Email: g.gharios{at}imperial.ac.uk

Received January 26, 2009. Revised June 6, 2009. Accepted June 10, 2009.

Transcriptional control of the genes coding for collagen type I is regulated by a complex interaction between a distal enhancer and a proximal promoter. In this study, we have dissected the molecular mechanism of this interaction by defining a specific sequence within the enhancer that respond in fibroblasts to transforming growth factor-β (TGF-β). We show that TGF-β activates COL1A2 gene via a non-canonical (Smad-independent) signalling pathway, which requires enhancer/promoter co-operation. This interaction involves exchange of cJun/Jun B transcription factor occupancy of a critical enhancer site resulting in the stabilization of enhancer/promoter coalescence. Moreover, using transgenesis, we show that interference in this mechanism results in the abolition of COL1A2 fibroblast expression in vivo. These data are therefore relevant to the control of collagen type I in vivo both in embryonic development, in adult connective tissue homeostasis, and in tissue repair and scarring pathologies.

The authors wish it to be known that, in their opinion, the last two authors should be regarded as joint Senior Authors.


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