Induced expression from the Moloney murine leukemia virus long terminal repeat during differentiation of human myeloid cells is mediated through its transcriptional enhancer.
Transcription from the Moloney murine leukemia virus (Mo-MuLV) long terminal repeat (LTR) is inhibited in murine stem cells and induced during maturation of these cells. We have investigated whether alterations in the activity of this viral regulatory element also occur during differentiation of human myeloid leukemia cells. The Mo-MuLV LTR and the simian virus 40 (SV40) early promoter were introduced into HL-60 promyelocytes on Epstein-Barr virus-derived chloramphenicol acetyltransferase expression vectors. When these cells were induced to terminally differentiate, transcription from the Mo-MuLV LTR was induced approximately 10-fold. Expression from the SV40 promoter remained constant during differentiation of these cells. Replacing the SV40 transcriptional enhancer with the Mo-MuLV LTR transcriptional enhancer rendered the SV40 promoter inducible during differentiation. We conclude that sequences within the transcriptional enhancer of the Mo-MuLV LTR contain cis-acting elements responsible for induction of gene expression during differentiation of human myeloid cells.
Reisman
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D
Department of Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Rotter
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V
D002454:Cell Differentiation; D002460:Cell Line; D015500:Chloramphenicol O-Acetyltransferase / Q000235:genetics; D004121:Dimethyl Sulfoxide / Q000494:pharmacology; D004742:Enhancer Elements, Genetic; D005786:Gene Expression Regulation; D005822:Genetic Vectors; D006098:Granulocytes / Q000378:metabolism*; D006801:Humans; D008979:Moloney murine leukemia virus / Q000235:genetics*; D011401:Promoter Regions, Genetic; D012313:RNA / Q000032:analysis; D013539:Simian virus 40 / Q000235:genetics
D012313:RNA; D015500:Chloramphenicol O-Acetyltransferase; D004121:Dimethyl Sulfoxide