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Papers In Press, published online ahead of print October 27, 2000
Terry Fox Laboratory, B. C. Cancer Agency, Vancouver, B.C. V5Z1L3
Corresponding Author: dixie{at}interchange.ubc.ca
To examine the potential regulatory involvement of retroelements in the human genome, we screened the transcribed sequences of GenBank and EST databases with long terminal repeat (LTR) elements derived from different human endogenous retroviruses (HERVs). These screenings detected human transcripts containing LTRs belonging to the HERV-E family fused to the apolipoprotein CI (APOCI) and the endothelin B receptor (EBR) genes. However, both genes are known to have non-LTR (native) promoters. Initial RT-PCR experiments confirmed and authenticated the presence of transcripts from both the native and LTR promoters. Using a 5' RACE protocol, we showed that the alternative transcripts of APOCI and EBR are initiated and promoted by the LTRs. The LTR-APOCI fusion and native APOCI transcripts are present in many of the tissues tested. As expected, we found APOCI preferentially expressed in liver, where ca 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 APOCI 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 APOCI, 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.
J. Biol. Chem, 10.1074/jbc.M006557200
Submitted on July 24, 2000
Revised on September 28, 2000
Accepted on October 26, 2000
Long terminal repeats are used as alternative promoters for the endothelin B receptor and apolipoprotein C-I genes in humans
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