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The role of the dioxin-responsive element cluster between the Cyp1a1 and Cyp1a2 loci in aryl hydrocarbon receptor biology
Abstract
The aryl hydrocarbon receptor (AHR) plays a central role in 2,3,7,8-tetrachlorodibenzo- p -dioxin (dioxin) hepatotoxicity, regulation of xenobiotic metabolism, and hepatovascular development. Each of these processes appears to be dependent on binding of the AHR to dioxin- responsive elements (DREs) within the genome. The Cyp1a1 and Cyp1a2 loci represent linked genes thought to play important roles in AHR biology. In the mouse, 8 DREs are located in the 14-kb intergenic region between the Cyp1a1 and Cyp1a2 genes. Seven of these DREs, collectively known as the DRE cluster (DREC), are located 1.4 kb upstream of the Cyp1a1 transcriptional start site and 12.6 kb upstream of the Cyp1a2 start site. To investigate the role of the DREC in each aspect of AHR biology, we generated a DREC-deficient mouse model through homologous recombination. Using this mouse model, we demonstrate that the DREC controls the adaptive up-regulation of both Cyp1a1 and Cyp1a2 genes in vivo. Using selected aspects of acute hepatic injury as endpoints, we also demonstrate that DREC null mice are more sensitive to dioxin-induced hepatotoxicity than WT mice. The results of parallel toxicologic studies using individual Cyp1a1 and Cyp1a2 null mice support the observation that up-regulation of these P450s is not the cause of many aspects of dioxin hepatotoxicity. Finally, we observed normal closure of the ductus venosus (DV) in DREC null mice. Given the 100% penetrance of patent DV in Ahr null mice, these results indicate that Cyp1a1 and Cyp1a2 do not play a dominant role in AHR-mediated vascular development.
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“This idea is supported by the emerging observation that many physiological consequences of Ahr deletion are absent in many Cyp1 knockout animals (McKinnon & Nebert, 1998; Nukaya et al., 2009).”
From Rodent Genetic Models of Ah Receptor Signaling (2021) · cites this paper as Nukaya et al., 2009
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The Aryl Hydrocarbon Receptor Complex
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“Evidence from recombinant mouse models supports the idea that the upstream signaling events are similar in the adaptive, toxic, and developmental pathways; that is, each pathway is dependent on chaperone binding by the AHR, activation of the AHR, dimerization of the AHR with ARNT, and the binding of this complex to ge…”
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Sorted by citations
van Voorhis, M., Knopp, S., Julliard, W., Fechner, J. H., Zhang, X., Schauer, J. J., & Mezrich, J. D. (2013) · PLoS ONE · doi:10.1371/journal.pone.0082545 · Cited by 145
Rodent Genetic Models of Ah Receptor Signaling
Wilson, R. H., & Bradfield, C. A. (2021) · Drug Metabolism Reviews · doi:10.1080/03602532.2021.1955916 · Cited by 16
“This idea is supported by the emerging observation that many physiological consequences of Ahr deletion are absent in Cyp1 knockout animals (McKinnon and Nebert 1998; Nukaya et al. 2009).”
BackgroundSelf-citation
Metadata
- Authors
- Nukaya, M., Moran, S., & Bradfield, C. A.
- Affiliations
- McArdle Laboratory for Cancer Research, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53706
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2009-03-24
- Volume
- 106
- Issue
- 12
- Pages
- 4923-4928
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 91
- References
- 5
- Language
- en
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