Key points are not available for this paper at this time.
The AH receptor is a ligand-activated transcription factor that mediates the biological effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin. The AH receptor has primary sequence homology to its dimerization partner the AH receptor nuclear translocator, and to the Drosophila proteins Sim and Per. Characterization of the gene encoding the murine AH receptor (Ahr gene) reveals that its structural organization is also conserved with respect to the sim gene, since 6 of 11 Ahr exons are spliced at homologous sites. Interestingly, little splicing homology was observed between the Ahr and per genes. The promoter of the Ahr gene is GC-rich and contains no TATA or CCAAT boxes; however, sequence analysis has shown several binding sites for the transcription factor Sp1 (GC boxes). Additionally we have identified a potential cAMP response element, AP-1 and E box sites, and two elements demonstrated in other genes to confer placenta-specific expression. Using a restriction fragment length polymorphism in exon 7 and recombinant inbred mouse lines, the Ahr gene was found to be concordant with the phenotypically defined Ahr locus, supporting the identity of these two genetic elements.
Schmidt et al. (Fri,) studied this question.