TitleTwo forms of aryl hydrocarbon receptor type 2 in rainbow trout (Oncorhynchus mykiss). Evidence for differential expression and enhancer specificity.
Publication TypeJournal Article
Year of Publication1999
AuthorsAbnet, CC, Tanguay, RL, Hahn, ME, Heideman, W, Peterson, RE
JournalJ Biol Chem
Volume274
Issue21
Pagination15159-66
Date Published1999 May 21
ISSN0021-9258
KeywordsAmino Acid Sequence, Animals, Cloning, Molecular, DNA, Complementary, Female, Molecular Sequence Data, Oncorhynchus mykiss, Polychlorinated Dibenzodioxins, Receptors, Aryl Hydrocarbon, RNA, Messenger, Transcription, Genetic
Abstract

Two aryl hydrocarbon receptors (AhRs), rtAhR2alpha and rtAhR2beta, were cloned from rainbow trout (rt) cDNA libraries. The distribution of sequence differences, genomic Southern blot analysis, and the presence of both transcripts in all individual rainbow trout examined suggest that the two forms of rtAhR2 are derived from separate genes. The two rtAhR2s have significant sequence similarity with AhRs cloned from mammalian species, especially in the basic helix-loop-helix and PAS functional domains located in the amino-terminal 400 amino acids of the protein. In contrast, the Gln-rich transactivation domain found in the carboxyl-terminal half of mammalian AhRs is absent from both rtAhR2s. Both clones were expressed by in vitro transcription/translation and proteins of approximately 125 kDa were produced. These proteins bind 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) and are able to bind dioxin response elements in gel shift assays. rtAhR2alpha and rtAhR2beta are expressed in a tissue-specific manner with the highest expression of rtAhR2beta in the heart. Expression of rtAhR2alpha and rtAhR2beta mRNAs is positively regulated by TCDD. Both rtAhR2alpha and rtAhR2beta produced TCDD-dependent activation of a reporter gene driven by dioxin response elements. Surprisingly, the two receptors showed distinct preferences for different enhancer sequences. These results suggest that the two receptor forms may regulate different sets of genes, and may play different roles in the toxic responses produced by AhR agonists such as TCDD.

Alternate JournalJ. Biol. Chem.
PubMed ID10329723
PubMed Central IDPMC2186364
Grant ListR01 ES006272-08 / ES / NIEHS NIH HHS / United States
R01 ES006272 / ES / NIEHS NIH HHS / United States
F32 ES05786-01 / ES / NIEHS NIH HHS / United States
R29 ES06272 / ES / NIEHS NIH HHS / United States
F32 ES005786-02 / ES / NIEHS NIH HHS / United States
F32 ES005786 / ES / NIEHS NIH HHS / United States