Aryl hydrocarbon receptor mediates larval zebrafish fin duplication following exposure to benzofluoranthenes.

Polycyclic aromatic hydrocarbons (PAHs) can alter gene expression by acting through the aryl hydrocarbon receptor (AHR). In a previous phenotypic screen of over 120 PAHs, we identified four PAHs that induce an ectopic caudal fin (called X-fin) in larval zebrafish: benzo[k]fluoranthene (BkF), dibenzo[b,k]fluoranthene, dibenzo[a,h]anthracene, and benzo[j]fluoranthene. We investigated several plausible mechanisms of X-fin formation using the most potent X-fin inducer, BkF. The X-fin phenotype was dependent on the AHR paralog Ahr2, and we performed RNA sequencing to identify altered gene expression patterns. Transcriptional profiles of distal trunk tissue, where the phenotype was manifest, were generated for animals exposed to 1% DMSO (control) or 12 µM BkF. Four time points of X-fin development were considered for transcriptomics: prior to visual emergence of X-fin (48 hpf), during manifestation of disrupted caudal fin fold development (60 and 72 hpf), and after emergence of X-fin (96 hpf). Overall design: RNA profiles of larval zebrafish trunk tissue at 48, 60, 72, and 96 hpf, from animals exposed to either 1% DMSO or 12 µM benzo[k]fluoranthene, were generated using Illumina HiSeq 2500 with 100 bp single end reads. There were n = 50 per bioreplicate and four bioreplcates per condition, totaling 32 raw samples. Each processed sample consists of mean normalized counts from four raw data files, totaling eight processed samples.