5-Azacytidine-induced reactivation of a herpes simplex thymidine kinase gene.
Mouse cells transformed with herpes simplex virus and containing the viral thymidine kinase (TK) gene in an inactive state were treated with 5-azacytidine. The result was the reexpression of the viral TK gene. Two days of exposure to 5-azacytidine followed by 2 days of expression time was sufficient for maximal induction of the TK+ phenotype. The induction of TK expression by 5-azacytidine was concentration-dependent, with maximal induction at 10 micromoles per liter. 5-Azacytidine also inhibited the decay of TK expression in TK+ transformants removed from selective conditions. Analysis of the methylation patterns of the viral TK gene with restriction endonucleases Hpa II and Msp I showed the active gene to be unmethylated, the inactive gene methylated, and the 5-azacytidine-induced gene unmethylated.
D001374:Azacitidine / Q000494:pharmacology*; D002472:Cell Transformation, Viral; D004247:DNA / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects*; D005814:Genes, Viral; D008745:Methylation; D018139:Simplexvirus / Q000235:genetics*; D013937:Thymidine Kinase / Q000235:genetics*
D004247:DNA; D013937:Thymidine Kinase; D001374:Azacitidine