REPRESSION OF RETINOIC ACID-INDUCED TRANSACTIVATION BY EMBRYONAL LTR BINDING-PROTEIN

The mechanism of repression of transcription by ELP, the embryonal lon g terminal repeat binding protein, was investigated. ELP represses the Moloney murine leukemia virus long terminal repeat by binding to a si te which overlaps with a sequence element for retinoic acid receptor b inding. This suggests possible competition of ELP with retinoic acid r eceptor for the same sequence elements. Oligonucleotides corresponding to ELP and/or retinoic acid receptor binding elements were placed ups tream of the SV40 promoter and their effect on gene expression was ana lyzed by CAT assay. Elements which have affinity to both ELP and retin oic acid receptor were activated by retinoic acid receptor and these a ctivations were repressed by ELP. An ELP binding element without affin ity to retinoic acid receptor was insensitive to both activation by re tinoic acid receptor and repression by ELP. Furthermore, cellular ELP binding elements and the Moloney leukemia virus long terminal repeat w ere activated by retinoic acid. These data suggest that one of the mec hanism of transcriptional repression by ELP is competition for binding sites with transactivators such as retinoic acid receptors.