Abstract
The expression of beta interferon genes from humans and mice is under the immediate control of a virus-responsive element (VRE) that terminates 110 bp upstream from the transcriptional start site. Whereas a wealth of information is available for the enhanceosome that is formed on the VRE upon the signals generated by viral infection, early observations indicating the existence of other far-upstream control elements have so far remained without a molecular fundament. Guided by a computational analysis of DNA structures, we could locate three as-yet-unknown transcription factor-binding regions at -0.5, -2, and -3 kb. Our present study delineates the interplay of factors YY1 and YY2 as it occurs at the sites at -3 kb and -2 kb (otherwise called HS1 and HS2), consistent with the idea that the novel factor YY2 antagonizes the negative actions exerted by YY1. Differences between the human and murine control regions will be described.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Base Sequence
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Binding Sites
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Cell Nucleus / metabolism
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Chromatin Immunoprecipitation
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Cloning, Molecular
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Computational Biology
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DNA / chemistry
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DNA, Complementary / metabolism
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Dose-Response Relationship, Drug
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Gene Expression Regulation*
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Genes, Reporter
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Humans
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Interferon-beta / genetics*
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Interferons / metabolism
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Luciferases / metabolism
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Mice
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Molecular Sequence Data
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Mutagenesis, Site-Directed
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Oligonucleotides / chemistry
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Plasmids / metabolism
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Promoter Regions, Genetic*
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Protein Binding
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Protein Biosynthesis
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Species Specificity
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Transcription Factors / genetics
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Transcription Factors / physiology*
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Transcription, Genetic
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Transfection
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Two-Hybrid System Techniques
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YY1 Transcription Factor / genetics
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YY1 Transcription Factor / physiology*
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beta-Galactosidase / metabolism
Substances
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DNA, Complementary
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Oligonucleotides
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Transcription Factors
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YY1 Transcription Factor
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YY1 protein, human
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YY2 protein, human
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Yy1 protein, mouse
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Interferon-beta
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DNA
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Interferons
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Luciferases
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beta-Galactosidase