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GENETICS
An endogenous retroviral long terminal repeat is the dominant promoter for human 1,3-galactosyltransferase 5 in the colon

Catherine A. Dunn ^* , Patrik Medstrand , and Dixie L. Mager ^*  

^*Terry Fox Laboratory, BC Cancer Agency, Vancouver, BC, Canada V5Z 1L3; Department of Cell and Molecular Biology, Biomedical Centre, Lund University, 221 84 Lund, Sweden; and Department of Medical Genetics, University of British Columbia, Vancouver, BC, Canada V6T 1Z1

Edited by Roy J. Britten, California Institute of Technology, Corona Del Mar, CA, and approved August 29, 2003 (received for review July 16, 2003)

LTRs of endogenous retroviruses are known to affect expression of several human genes, typically as a relatively minor alternative promoter. Here, we report that an endogenous retrovirus LTR acts as one of at least two alternative promoters for the human 1,3-galactosyltransferase 5 gene, involved in type 1 Lewis antigen synthesis, and show that the LTR promoter is most active in the gastrointestinal tract and mammary gland. Indeed, the LTR is the dominant promoter in the colon, indicating that this ancient retroviral element has a major impact on gene expression. Using colorectal cancer cell lines and electrophoretic mobility-shift assays, we found that hepatocyte nuclear factor 1 (HNF-1) binds a site within the retroviral promoter and that expression of HNF-1 and interaction with its binding site correlated with promoter activation. We conclude that HNF-1 is at least partially responsible for the tissue-specific activation of the LTR promoter of human 1,3-galactosyltransferase 5. We demonstrate that this tissue-specific transcription factor is implicated in the activation of an LTR gene promoter.

Abbreviations: 3Gal-T5, 1,3-galactosyltransferase 5; HERV, human endogenous retrovirus; HNF-1, hepatocyte nuclear factor 1.

Data deposition: The sequence reported in this paper has been deposited in the GenBank database (accession no. AY372061).

To whom correspondence should be addressed. E-mail: dmager{at}bccrc.ca.

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