A structurally diverse group of chemicals, including dioxins [e.g., 2,3,7,8-tetrachlorodibenzo-<i>p</i>-dioxin (TCDD)] and polycyclic aromatic hydrocarbons (PAHs), can xenobiotically activate the aryl hydrocarbon receptor (AHR) and contribute to adverse health effects in humans and wildlife. In the zebrafish model, repression of <i>sox9b</i> has a causal role in several AHR-mediated toxic responses, including craniofacial cartilage malformations; however, the mechanism of <i>sox9b</i> repression remains unknown. We previously identified a long noncoding RNA, <i>sox9b</i> long intergenic noncoding RNA (<i>slincR</i>), which is increased (in an AHR-dependent manner) by multiple AHR ligands and is required for the AHR-activated repression of <i>sox9b</i>.
