Subfragments of the large terminal repeat cause glucocorticoid-responsive expression of mouse mammary tumor virus and of an adjacent gene.
After transfection of mouse mammary tumor virus (MMTV) proviral DNA into cultured cells, the DNA is transcribed in a glucocorticoid-sensitive fashion. The large terminal repeat (LTR) region of MMTV is 1,328 nucleotides long and contains the regulatory information necessary for the hormonal response. We have constructed a MMTV LTR-thymidine kinase (tk) chimeric gene and have tested the biological activity of molecules containing various deletions in the LTR after transformation of LTK- APRT- mouse cells. In the TK+ transformants, both a LTR- tk chimeric RNA and an authentic tk RNA are correctly initiated and transcribed. The synthesis of the chimeric RNA as well as that of the tk RNA is hormonally regulated. A plasmid containing 202 nucleotides of LTR DNA 5' to the RNA initiation site is fully sensitive to glucocorticoids; 50 nucleotides still cause a residual inducibility.
D002471:Cell Transformation, Neoplastic; D004262:DNA Restriction Enzymes; D005796:Genes / Q000187:drug effects*; D005814:Genes, Viral / Q000187:drug effects*; D005938:Glucocorticoids / Q000494:pharmacology*; D008324:Mammary Tumor Virus, Mouse / Q000187:drug effects / Q000235:genetics*; D010957:Plasmids; D013937:Thymidine Kinase / Q000235:genetics; D014158:Transcription, Genetic / Q000187:drug effects*
D005938:Glucocorticoids; D013937:Thymidine Kinase; D004262:DNA Restriction Enzymes