Atlantic killifish (Fundulus heteroclitus) residing in some urban and industrialized estuaries of the US eastern seaboard demonstrate recently evolved and extreme tolerance to toxic aryl hydrocarbon pollutants, characterized as dioxin-like compounds (DLCs). Here, we provide an unusually comprehensive accounting (69%) through quantitative trait locus (QTL) analysis of the genetic basis for DLC tolerance in killifish inhabiting an urban estuary contaminated with PCB congeners, the most toxic of which are DLCs. Consistent with mechanistic knowledge of DLC toxicity in fish and other vertebrates, the aryl hydrocarbon receptor (ahr2) region accounts for 17% of trait variation; however, QTL on independent linkage groups and their interactions have even greater explanatory power (44%). QTL interpreted within the context of recently available Fundulus genomic resources and shared synteny among fish species suggest adaptation via interacting components of a complex stress response network. Some QTL were also enriched in other killifish populations characterized as DLC-tolerant and residing in distant urban estuaries contaminated with unique mixtures of pollutants. Together, our results suggest that DLC tolerance in killifish represents an emerging example of parallel contemporary evolution that has been driven by intense human-mediated selection on natural populations.

The present study was undertaken to provide the foundation for development of genome‐scale resources for the fathead minnow (Pimephales promelas), an important model organism widely used in both aquatic toxicology research and regulatory testing. The authors report on the first sequencing and 2 draft assemblies for the reference genome of this species. Approximately 120× sequence coverage was achieved via Illumina sequencing of a combination of paired‐end, mate‐pair, and fosmid libraries. Evaluation and comparison of these assemblies demonstrate that they are of sufficient quality to be useful for genome‐enabled studies, with 418 of 458 (91%) conserved eukaryotic genes mapping to at least 1 of the assemblies. In addition to its immediate utility, the present work provides a strong foundation on which to build further refinements of a reference genome for the fathead minnow. Environ Toxicol Chem 2016;35:212–217. © 2015 SETAC

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Variability in risk of developmental defects caused by dioxin-like compounds (DLCs) has been demonstrated within and among several vertebrate species. Beyond our knowledge of the aryl hydrocarbon receptor (AHR) and its role in mediating toxicity for this class of compounds, little else is known concerning precise downstream targets influencing this vulnerability. In the present study, zebrafish with divergent genetic backgrounds were screened for susceptibility to developmental cardiotoxicity caused by the prototypical DLC, 3,3',4,4',5-pentachlorobiphenyl (PCB126); a range up to ∼40-fold differences was observed. Differentially sensitive zebrafish were chosen for a genetic cross, and the recombinant generation was used for genome-wide quantitative trait loci (QTL) mapping. Multiple QTLs were identified--several acting alone, one additively, and two others via epistatic interaction. Together, these QTLs account for 24% of the phenotypic variance observed in cardioteratogenicity resulting from PCB126 exposure (logarithm of the odds = 13.55, p = 1.89 × 10⁻¹⁰). Candidate genes in these QTL regions include the following: ahr2, bcor, and capn1 (Chr 22); e2f1 and pdyn (Chr 23); ctnnt2, plcg1, eno3, tgm1, and tgm2 (interacting on Chr 23); and vezf1 (Chr 15). These data demonstrate that DLC-induced cardiac teratogenicity is a multifactorial complex trait influenced by gene × gene and gene × environment interactions. The identified QTLs harbor many DLC-responsive genes critical to cardiovascular development and provide insight into the genetic basis of susceptibility to AHR-mediated developmental toxicity.

1. The influence of spatial structure on population dynamics within river-stream networks is poorly understood. Utilizing spatially explicit analyses of temporal genetic variance, we tested whether persistence of central stonerollers (Campostoma anomalum) reflects differences in habitat quality and location within a highly modified urban catchment in southwestern Ohio, U.S.A. 2. Estimates of genetic diversity did not vary with habitat quality. Nevertheless, evidence of weak but temporally stable genetic structure, location-dependent effective population sizes and rates of immigration among sites, together suggest that persistence of central stonerollers within the catchment may be attributable to source-sink dynamics driven by habitat heterogeneity. 3. Under this scenario, migrant-pool colonization from areas of relatively high habitat quality in the upper catchment sustains the presence of central stonerollers at degraded sites in the main stem and dampens population subdivision within the catchment. However, because intact habitat is restricted to the upper portion of the catchment, it is not possible to preclude net downstream dispersal as a mechanism contributing to sourcesink dynamics. The slight genetic structure that persists appears to reflect weak isolation by distance diminished by high rates of immigration. 4. This study suggests that without a systems perspective of the conditions that sustain populations in degraded waterways, environmental assessments may underestimate levels of impairment. Conservation and management of stream fishes could be improved by maintaining habitat in areas that are net exporters of migrants or by remediation of impaired habitat.