The mammalian aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates the toxic effects of dioxins and related compounds. Dioxins have been shown to cause a range of neurological defects, but the role of AHR during normal neuronal development is not known. Here we investigate the developmental functions of
ahr-1, the Caenorhabditis elegans aryl hydrocarbon receptor homolog. We show that
ahr-1:GFP is expressed in a subset of neurons, and we demonstrate that 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. In
ahr-1-deficient animals, the touch receptor neuron AVM and its sister cell, the interneuron SDQR, exhibit cell and axonal migration defects. We show that dorsal migration of SDQR is mediated by UNC-6/Netrin, SAX-3/Robo, and UNC-129/TGFbeta, and this process requires the functions of both
ahr-1 and its transcription factor dimerization partner
aha-1. We also document a role for
ahr-1 during the differentiation of the neurons that contact th