Activation of the human beta-interferon gene requires an interferon-inducible factor.
beta-Interferon (beta-IFN) gene expression can be induced by poly(I)-poly(C) or virus, but there is considerable variation in the extent of induction between different cell lines. We characterized two poorly inducible human cell lines, HeLa and 143 thymidine kinase negative (143 tk-), to define cellular factors involved in the activation of the beta-IFN gene. We show that the deficiency in beta-IFN induction in these cells can be complemented by fusion to highly inducible mouse cells. We conclude that the human cells are deficient in a trans-acting factor required for B-IFN gene activation. The level of induction of the beta-IFN gene in HeLa and 143 tk- cells can also be increased by priming with IFN before induction. If IFN priming is carried out in the presence of cycloheximide, a approximately 200-fold increase in induction is observed. We conclude that activation of the beta-IFN gene requires an IFN-inducible factor that is only expressed at low levels in unprimed HeLa and 143 tk- cells.
D002459:Cell Fusion; D002460:Cell Line; D003513:Cycloheximide / Q000494:pharmacology; D005796:Genes / Q000187:drug effects*; D005809:Genes, Regulator / Q000187:drug effects; D006367:HeLa Cells / Q000187:drug effects; D006801:Humans; D007370:Interferon Type I / Q000096:biosynthesis / Q000235:genetics*; D009693:Nucleic Acid Hybridization; D010957:Plasmids; D011070:Poly I-C / Q000494:pharmacology*; D013937:Thymidine Kinase / Q000235:genetics; D014158:Transcription, Genetic / Q000187:drug effects*
D007370:Interferon Type I; D003513:Cycloheximide; D013937:Thymidine Kinase; D011070:Poly I-C