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Originally published In Press as doi:10.1074/jbc.M006557200 on October 27, 2000

J. Biol. Chem., Vol. 276, Issue 3, 1896-1903, January 19, 2001
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Long Terminal Repeats Are Used as Alternative Promoters for the Endothelin B Receptor and Apolipoprotein C-I Genes in Humans*

Patrik MedstrandDagger , Josette-Renée Landry§, and Dixie L. Mager

From the Terry Fox Laboratory, British Columbia Cancer Agency and Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, V5Z 1L3, Canada

To examine the potential regulatory involvement of retroelements in the human genome, we screened the transcribed sequences of GenBankTM and expressed sequence tag data bases with long terminal repeat (LTR) elements derived from different human endogenous retroviruses. These screenings detected human transcripts containing LTRs belonging to the human endogenous retrovirus-E family fused to the apolipoprotein CI (apoC-I) and the endothelin B receptor (EBR) genes. However, both genes are known to have non-LTR (native) promoters. Initial reverse transcription-polymerase chain reaction experiments confirmed and authenticated the presence of transcripts from both the native and LTR promoters. Using a 5'-rapid amplification of cDNA ends protocol, we showed that the alternative transcripts of apoC-I and EBR are initiated and promoted by the LTRs. The LTR-apoC-I fusion and native apoC-I transcripts are present in many of the tissues tested. As expected, we found apoC-I preferentially expressed in liver, where about 15% of the transcripts are derived from the LTR promoter. Transient transfections suggest that the expression is not dependent on the LTR itself, but the presence of the LTR increases activity of the apoC-I promoter from both humans and baboons. The native EBR-driven transcripts were also detected in many tissues, whereas the LTR-driven transcripts appear limited to placenta. In contrast to the LTR of apoC-I, the EBR LTR promotes a significant proportion of the total EBR transcripts, and transient transfection results indicate that the LTR acts as a strong promoter and enhancer in a placental cell line. This investigation reports two examples where LTR sequences contribute to increased transcription of human genes and illustrates the impact of mobile elements on gene and genome evolution.

* This work was supported by a grant from the Medical Research Council (MRC) of Canada with core support provided by the British Columbia Cancer Agency, by the Crafoord Foundation and the Royal Physiografic Foundation, Lund, Sweden.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger Supported by a fellowship from the Swedish Cancer Foundation and Knut and Alice Wallenberg Foundation, Sweden.

§ Supported by a studentship from the MRC of Canada.

To whom correspondence should be addressed: Terry Fox Laboratory, BC Cancer Agency, 601 West 10th Ave., Vancouver, British Columbia V5Z 1L3, Canada. Tel.: 604-877-6070 (ext. 3185); Fax: 604-877-0712; E-mail: dixie@interchange.ubc.ca.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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