Reticuloendotheliosis virus long terminal repeat elements are efficient promoters in cells of various species and tissue origin, including human lymphoid cells.
Promiscuous transcriptional activity of the reticuloendotheliosis virus (REV) long terminal repeat (LTR) was detected in transient expression assays using LTR-chloramphenicol acetyltransferase-encoding gene chimeras, and cells of diverse species and tissue type; levels of expression from two different REV LTRs correlate with reports of pathogenicity of the respective viruses in vivo. REVs do not encode a transactivator targeted to the viral LTR, and cells infected with Marek's disease virus, a herpesvirus with an overlapping host range, do not express factors that preferentially enhance expression from REV or avian sarcoma/leukemia virus LTRs. REV LTRs work efficiently in human lymphoid cells, and are viable alternatives to promoters commonly used for expression of cloned genes. They may also prove useful in the identification of new, ubiquitous cellular transcription factors.
Ridgway
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Department of Microbiology and Immunology, University of Western Ontario, London, Canada.
D000818:Animals; D002478:Cells, Cultured; D002645:Chickens; D004285:Dogs; D015967:Gene Expression Regulation, Viral; D006801:Humans; D066298:In Vitro Techniques; D008214:Lymphocytes / Q000502:physiology; D011401:Promoter Regions, Genetic; D012091:Repetitive Sequences, Nucleic Acid; D001356:Reticuloendotheliosis virus / Q000235:genetics*; D013539:Simian virus 40 / Q000235:genetics; D014157:Transcription Factors / Q000502:physiology
D014157:Transcription Factors