SREL Reprint #3555

AHR and CYP1A expression link historical contamination events to modern day developmental effects in the American alligator

Matthew D. Hale1,2, Thomas M. Galligan3, Thomas R. Rainwater4, Brandon C. Moore5,
Philip M. Wilkinson6, Louis J. Guillette3, and Benjamin B. Parrott1,2

1Savannah River Ecology Laboratory, P.O. Drawer E, Aiken, SC 29802, United States
2Odum School of Ecology, University of Georgia, Athens, GA 30602, United States
3Marine Biomedicine and Environmental Sciences Program, Hollings Marine Laboratory and the Medical University of South Carolina, Charleston, SC 29412, United States
4Tom Yawkey Wildlife Center & Belle W. Baruch Institute of Coastal Ecology and Forest Science,
Clemson University, Georgetown, SC 29442, United States
5Department of Biology, Sewanee: the University of the South, Sewanee, TN 37383, United States
6Tom Yawkey Wildlife Center Heritage Preserve, South Carolina Department of Natural Resources,
Georgetown, SC 29440, United States

Abstract: The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that initiates a transcriptional pathway responsible for the expression of CYP1A subfamily members, key to the metabolism of xenobiotic compounds. Toxic planar halogenated aromatic hydrocarbons, including dioxin and PCBs, are capable of activating the AHR, and while dioxin and PCB inputs into the environment have been dramatically curbed following strict regulatory efforts in the United States, they persist in the environment and exposures remain relevant today. Little is known regarding the effects that long-term chronic exposures to dioxin or dioxin-like compounds might have on the development and subsequent health of offspring from exposed individuals, nor is much known regarding AHR expression in reptilians. Here, we characterize AHR and CYP1A gene expression in embryonic and juvenile specimen of a long-lived, apex predator, the American alligator (Alligator mississippiensis), and investigate variation in gene expression profiles in offspring collected from sites conveying differential exposures to environmental contaminants. Both age- and tissue-dependent patterning of AHR isoform expression are detected. We characterize two downstream transcriptional targets of the AHR, CYP1A1 and CYP1A2, and describe conserved elements of their genomic architecture. When comparisons across different sites are made, hepatic expression of CYP1A2, a direct target of the AHR, appears elevated in embryos from a site associated with a dioxin point source and previously characterized PCB contamination. Elevated CYP1A2 expression is not persistent, as site-specific variation was absent in juveniles originating from field-collected eggs but reared under lab conditions. Our results illustrate the patterning of AHR gene expression in a long-lived environmental model species, and indicate a potential contemporary influence of historical contamination. This research presents a novel opportunity to link contamination events to critical genetic pathways during embryonic development, and carries significant potential to inform our understanding of potential health effects in wildlife and humans.

Keywords: Arylhydrocarbon receptor; Alligator; Polychlorinated biphenyl; Dioxin; Embryo; Cytochrome P450

SREL Reprint #3555

Hale, M. D., T. M. Galligan, T. R. Rainwater, B. C. Moore, P. M. Wilkinson, L. J. Guillette, and B. B. Parrott. 2017. AHR and CYP1A expression link historical contamination events to modern day developmental effects in the American alligator. Environmental Pollution 230(2017): 1050-1061.

This information was provided by the University of Georgia's Savannah River Ecology Laboratory (srel.uga.edu).