Abstract
BackgroundThe most toxic aromatic hydrocarbon pollutants are categorized as dioxin-like compounds (DLCs) to which extreme tolerance has evolved independently and contemporaneously in (at least) four populations of Atlantic killifish (Fundulus heteroclitus). Surprisingly, the magnitude and phenotype of DLC tolerance is similar among these killifish populations that have adapted to varied, but highly aromatic hydrocarbon-contaminated urban/industrialized estuaries of the US Atlantic coast. Multiple tolerant and neighboring sensitive killifish populations were compared with the expectation that genetic loci associated with DLC tolerance would be revealed.ResultsSince the aryl hydrocarbon receptor (AHR) pathway partly or fully mediates DLC toxicity in vertebrates, single nucleotide polymorphisms (SNPs) from 42 genes associated with the AHR pathway were identified to serve as targeted markers. Wild fish (N = 36/37) from four highly tolerant killifish populations and four nearby sensitive populations were genotyped using 59 SNP markers. Similar to other killifish population genetic analyses, strong genetic differentiation among populations was detected, consistent with isolation by distance models. When DLC-sensitive populations were pooled and compared to pooled DLC-tolerant populations, multi-locus analyses did not distinguish the two groups. However, pairwise comparisons of nearby tolerant and sensitive populations revealed high differentiation among sensitive and tolerant populations at these specific loci: AHR 1 and 2, cathepsin Z, the cytochrome P450s (CYP1A and 3A30), and the NADH dehydrogenase subunits. In addition, significant shifts in minor allele frequency were observed at AHR2 and CYP1A loci across most sensitive/tolerant pairs, but only AHR2 exhibited shifts in the same direction across all pairs.ConclusionsThe observed differences in allelic composition at the AHR2 and CYP1A SNP loci were identified as significant among paired sensitive/tolerant populations of Atlantic killifish with multiple statistical tests. The genetic patterns reported here lend support to the argument that AHR2 and CYP1A play a role in the adaptive response to extreme DLC contamination. Additional functional assays are required to isolate the exact mechanism of DLC tolerance.
Highlights
The most toxic aromatic hydrocarbon pollutants are categorized as dioxin-like compounds (DLCs) to which extreme tolerance has evolved independently and contemporaneously in four populations of Atlantic killifish (Fundulus heteroclitus)
Studies investigating the genetic basis for DLC-tolerance in zebrafish and Atlantic tomcod have isolated an AHR2 gene as a key player in mediating DLC sensitivity [6,48]; while AHR1 and AHR2 seem to play functional roles in dioxin toxicity in red seabream [35]. These results suggest that AHR2 variation likely plays a strong role in DLC sensitivity and tolerance in killifish, but more complex interactions may be revealed as new aryl hydrocarbon receptor (AHR) paralogs are being identified and characterized [9]
The purpose of this study was to identify genetic polymorphisms associated with DLC sensitivity in Atlantic killifish from a suite of candidate loci involved in the AHR and interacting pathways; whether the polymorphisms in and of themselves are responsible for the drastic differences in DLC sensitivity among populations was beyond the scope of this work
Summary
The most toxic aromatic hydrocarbon pollutants are categorized as dioxin-like compounds (DLCs) to which extreme tolerance has evolved independently and contemporaneously in (at least) four populations of Atlantic killifish (Fundulus heteroclitus). The early life stages of fish are sensitive to these toxic DLCs, and the Atlantic killifish, Fundulus heteroclitus, is one of the more sensitive fish species [1] Despite this species’ relative sensitivity to DLC exposure, several wild killifish populations residing in heavily contaminated North American Atlantic coast estuaries have recently and independently evolved dramatic, heritable, and adaptive tolerance to DLCs [2], for which the mechanistic basis has yet to be fully explained. To address this issue, a targeted, candidate gene scan was performed to reveal genetic variation associated with tolerance in four wild DLC-adapted killifish populations. The striking difference in DLC sensitivity among wild Atlantic tomcod populations has been attributed to a six base pair deletion in the AHR2 gene that results in a five-fold decrease in ligand binding affinity and reduced ability to promote expression of detoxification enzymes targeted by the AHR pathway [6]
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