
Contacts between hormone receptor and DNA double helix within a glucocorticoid regulatory element of mouse mammary tumor virus.
Author(s) -
Claus Scheidereit,
Miguel Beato
Publication year - 1984
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.81.10.3029
Subject(s) - biology , mouse mammary tumor virus , gene , long terminal repeat , hormone response element , glucocorticoid receptor , rous sarcoma virus , nuclear receptor , regulatory sequence , microbiology and biotechnology , transcription (linguistics) , transcription factor , genetics , gene expression , estrogen receptor , linguistics , philosophy , cancer , breast cancer
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 5'-T-G-T-T-C-T-3' 3'-A-C-A-A-G-A-5' 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 delta gag- mht gene, which is closely related to the delta 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.