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# Contacts between Hormone Receptor and DNA Double Helix within a Glucocorticoid Regulatory Element of Mouse Mammary Tumor Virus

Claus Scheidereit and Miguel Beato
Proceedings of the National Academy of Sciences of the United States of America
Vol. 81, No. 10, [Part 1: Biological Sciences] (May 15, 1984), pp. 3029-3033
Stable URL: http://www.jstor.org/stable/23620
Page Count: 5
Glucocorticoid hormones enhance the transcription of mouse mammary tumor virus DNA by mechanisms involving a direct interaction of the hormone receptor with four binding sites in a glucocorticoid regulatory element located between -72 and -192 base pairs upstream of the main transcription initiation site within the proviral long terminal repeat regions. Methylation at the N-7 position of any of three G residues within one of the binding sites prevents binding of the receptor. In addition, in the presence of the receptor, methylation by dimethyl sulfate is reduced at several G residues, indicating sites of contact between the receptor and DNA at these positions. The G residues in the hexanucleotide $\smallmatrix 5^{\prime}\text{-T-G-T-T-C-T-}3^{\prime} \\ 3^{\prime}\text{-A-C-A-A-G-A-}5^{\prime} \endsmallmatrix$were protected by the receptor against MH2-specific gene. (iii) myc is followed by the 3′-terminal c region of about 400 nucleotides, which is colinear with that of Rous sarcoma virus except for a substitution near the 5′ end of the long terminal repeat. It is concluded that MH2 contains two genes with oncogenic potential, the Δ gag-mht gene, which is closely related to the δ gag-raf transforming gene of MSV 3611, and the myc gene, which is related to the transforming gene of MC29. Furthermore, it may be concluded that the cellular proto-onc genes, which on sequence transduction become viral onc genes, are a small group because among the 19 known onc sequences, 5 are shared by different taxonomic groups of viruses of which the mht/raf homology is the closest determined so far.