Abstract
The winter flounder antifreeze protein (AFP) intron contains a liver-specific enhancer (Element B) which was shown earlier to bind CCAAT/enhancer binding protein (C/EBP)α. In contrast, as demonstrated in the present studies, the intron of the skin-type AFP gene acted as a ubiquitous enhancer and contained a TA insertion at similar region to Element B (Element S) which destroyed its interaction with C/EBPα. Furthermore, a TA insertion of Element B by site-directed mutagenesis decreased its liver enhancer activity. The presence or absence of C/EBPα binding motifs in Element B and Element S, respectively, may provide a mechanism for their differential expression.
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