DHR96 might be activated by phenobarbital, while AhR - only by planar PAHs and dioxins. So, DHR96 might be a predecessor for the AhR able to be activated by bulky and less hydrophobic xenobiotics.
Dear Fanny,
It's fanny (sorry for a calambur), but my point was not about orthologs well known from PUBMED' IDs. It was rather about archaic xenobiotics metabolism, induction of which might be viewed as an effective means of survival during evolution. In an ancient “fauna-flora war”, when presented with a life-threatening chemicals (namely, planar toxins developed by plants in order to avoid being eaten by giant animals), the cells processed with developing ligand-activated Ah receptor transcriptional machinery encoding CYP1As able to metabolize and detoxify planar xenobiotics (please learn more from Drs. Daniel Nebert and Allan Okey).
As for the DHR96 ortholog, a constitutive CAR, it was shown to activate its response element in a ligand-independent manner. The identity of CAR as a xenobiotic receptor was suggested when CAR was shown to activate the phenobarbital response element found in promoters of PB-inducible CYP2B genes.
On the other hand, the aryl hydrocarbon receptor (AhR) is a ligand-activated transcriptional factor. Although dioxin is high affinity and toxic to many vertebrate animals, invertebrate AhRs including Drosophila melanogaster AhR (spineless) have no ability to bind exogenous chemicals as ligands.
Best wishes,
Ilya
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