ArticleBMC evolutionary biology2014
Targeted approach to identify genetic loci associated with evolved dioxin tolerance in Atlantic killifish (Fundulus heteroclitus).
Article in BMC evolutionary biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Independently evolved pollution resistance in four killifish populations is largely explained by few variants of large effect.Evolutionary applications · 2024Article
- Urbanization and distance shape population structure inJournal of urban ecology · 2024Article
- Evidence of micro-evolution in Crocidura russula from two abandoned heavy metal mines: potential use of Cytb, CYP1A1, and p53 as gene biomarkers.Ecotoxicology (London, England) · 2021Article
- Resistance to Cyp3a induction by polychlorinated biphenyls, including non-dioxin-like PCB153, in gills of killifish (Fundulus heteroclitus) from New Bedford Harbor.Environmental toxicology and pharmacology · 2021Article
- Evolutionary Toxicology-An Informational Tool for Chemical Regulation?Environmental toxicology and chemistry · 2020Article
- Tributyltin disrupts fin development in Fundulus heteroclitus from both PCB-sensitive and resistant populations: Investigations of potential interactions between AHR and PPARγ.Aquatic toxicology (Amsterdam, Netherlands) · 2020Article
- Genetically inherited tolerance may unveil trait dominance patterns in an amphibian model.Scientific reports · 2019Article
- Characterization of the Fundulus heteroclitus embryo transcriptional response and development of a gene expression-based fingerprint of exposure for the alternative flame retardant, TBPH (bis (2-ethylhexyl)-tetrabromophthalate).Environmental pollution (Barking, Essex : 1987) · 2019Article
- Evolutionary Toxicogenomics of the Striped Killifish (International journal of molecular sciences · 2019Article
- Hepatic metabolite profiling of polychlorinated biphenyl (PCB)-resistant and sensitive populations of Atlantic killifish (Fundulus heteroclitus).Aquatic toxicology (Amsterdam, Netherlands) · 2018Article
- Genome-wide scan reveals signatures of selection related to pollution adaptation in non-model estuarine Atlantic killifish (Fundulus heteroclitus).Aquatic toxicology (Amsterdam, Netherlands) · 2018Article
- When evolution is the solution to pollution: Key principles, and lessons from rapid repeated adaptation of killifish (Evolutionary applications · 2017Review
- Adaptive capabilities and fitness consequences associated with pollution exposure in fish.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- The genomic landscape of rapid repeated evolutionary adaptation to toxic pollution in wild fish.Science (New York, N.Y.) · 2016Article
- Dioxin risk assessment: mechanisms of action and possible toxicity in human health.Environmental science and pollution research international · 2015Review
- Integrated ecological risk assessment of dioxin compounds.Environmental science and pollution research international · 2015Review
- Regulation of pregnane-X-receptor, CYP3A and P-glycoprotein genes in the PCB-resistant killifish (Fundulus heteroclitus) population from New Bedford Harbor.Aquatic toxicology (Amsterdam, Netherlands) · 2015Article
- Cloning of multiple ERα mRNA variants in killifish (Fundulus heteroclitus), and differential expression by tissue type, stage of reproduction, and estrogen exposure in fish from polluted and unpolluted environments.Aquatic toxicology (Amsterdam, Netherlands) · 2015Article
- The Elizabeth River Story: A Case Study in Evolutionary Toxicology.Journal of toxicology and environmental health. Part B, Critical reviews · 2015Review
- Genetic variation at aryl hydrocarbon receptor (AHR) loci in populations of Atlantic killifish (Fundulus heteroclitus) inhabiting polluted and reference habitats.BMC evolutionary biology · 2014Article
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4 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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