Background: The mammalian aryl hydrocarbon receptor mediates the toxic effects of dioxins.
Dioxins and related manmade pollutants are important hazards to human and animal health. People exposed to dioxin often have a skin condition called chloracne, and experiments in animal model systems suggest that dioxin exposure can also cause birth defects, cancer, and neurological defects. The toxic effects of dioxin are mediated by the aryl hydrocarbon receptor (AHR). Dioxin binds to AHR, causing misregulation of this protein.

Caenorhabditis elegans
C. elegans is a powerful genetic model system. The adults are approximately one millimeter long, and they eat bacteria. C. elegans are transparent. The wild-type embryonic and postembryonic lineages have been extensively documented and are essentially invariant. The nervous system consists of 302 neurons of at least 118 subtypes, and the neuronal connections have been reconstructed from serial section electron micrographs (www.wormatlas.org). These resources enable researchers to diagnose mutant phenotypes at the level of individual cells. The sequence of the genome is known (www.wormbase.org), and large-scale studies are underway to characterize the function of every gene by double-stranded RNA interference, full-genome microarrays, and semi-automated analyses of protein-protein interactions.

AHR signaling in C. elegans
The C. elegans orthologs of AHR and it’s dimerization partners are encoded by the genes ahr-1 and aha-1, respectively. The gene products, AHR-1 and AHA-1, share important biochemical properties with their mammalian cognates. There are also interesting differences. Like other invertebrate AHR homologs that have been tested, C. elegans AHR-1 does not bind radiolabeled derivatives of TCDD or beta-naphthoflavone. This suggests that evolutionary divergent AHR proteins recognize different spectrums of ligands or have varying mechanisms of activation. Powell-Coffman, Bradfield, and Wood (1998) PNAS 95, 2844

C. elegans ahr-1 is required for normal neuronal development.
ahr-1:GFP reporters are expressed in a subset of neurons. Animals lacking ahr-1 function have specific defects in neuronal differentiation, as evidenced by changes in gene expression, aberrant cell migration, axon branching, or supernumerary neuronal processes. These data, when considered with the neurotoxic effects of AHR-activating pollutants, support the hypothesis that AHR has an evolutionarily conserved role in neuronal development.
Qin and Powell-Coffman (2004) Dev. Biol. 270, 64

The C. elegans AHR-1 transcription complex regulates aggregation behavior.
Behavioral defects are evident in C. elegans lacking ahr-1. Some strains of C. elegans aggregate on lawns of bacterial food. This behavior is modulated by nutritional cues and ambient oxygen levels, and aggregation is inhibited by the npr-1 G protein-coupled neuropeptide receptor gene. We discovered that loss-of-function mutations in ahr-1 or its transcription partner aha-1 (ARNT) suppressed aggregation behavior in npr-1-deficient animals. This behavioral defect was not irreparable. Aggregation behavior could be restored to ahr-1-deficient animals by heat-shock induction of ahr-1 expression in larvae. Our data support a model in which the AHR-1:AHA-1 transcription complex regulates the expression of soluble guanylate cyclase genes and other unidentified genes that are essential for acute regulation of aggregation behavior. Qin, Zhai, and Powell-Coffman (2006) Dev. Biol. 298, 606