Dataset Information

Evolutionary Toxicogenomics of the Striped Killifish (Fundulus majalis) in the New Bedford Harbor (Massachusetts, USA).

ABSTRACT: In this paper, we used a Genotyping-by-Sequencing (GBS) approach to find and genotype more than 4000 genome-wide SNPs (Single Nucleotide Polymorphisms) from striped killifish exposed to a variety of polychlorinated biphenyls (PCBs) and other aromatic pollutants in New Bedford Harbor (NBH, Massachusetts, USA). The aims of this study were to identify the genetic consequences of exposure to aquatic pollutants and detect genes that may be under selection. Low genetic diversity (HE and ?) was found in the site exposed to the highest pollution level, but the pattern of genetic diversity did not match the pollution levels. Extensive connectivity was detected among sampling sites, which suggests that balanced gene flow may explain the lack of genetic variation in response to pollution levels. Tests for selection identified 539 candidate outliers, but many of the candidate outliers were not shared among tests. Differences among test results likely reflect different test assumptions and the complex pollutant mixture. Potentially, selectively important loci are associated with 151 SNPs, and enrichment analysis suggests a likely involvement of these genes with pollutants that occur in NBH. This result suggests that selective processes at genes targeted by pollutants may be occurring, even at a small geographical scale, and may allow the local striped killifish to resist the high pollution levels.

SUBMITTER: Ruggeri P

PROVIDER: S-EPMC6429206 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature

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Evolutionary Toxicogenomics of the Striped Killifish (Fundulus majalis) in the New Bedford Harbor (Massachusetts, USA).

Ruggeri Paolo P Du Xiao X Crawford Douglas L DL Oleksiak Marjorie F MF

International journal of molecular sciences 20190305 5

In this paper, we used a Genotyping-by-Sequencing (GBS) approach to find and genotype more than 4000 genome-wide SNPs (Single Nucleotide Polymorphisms) from striped killifish exposed to a variety of polychlorinated biphenyls (PCBs) and other aromatic pollutants in New Bedford Harbor (NBH, Massachusetts, USA). The aims of this study were to identify the genetic consequences of exposure to aquatic pollutants and detect genes that may be under selection. Low genetic diversity (HE ...[more]

PMID: 30841640

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Project description:Sentinel species such as the Atlantic killifish (Fundulus heteroclitus) living in urban waterways can be used as toxicological models to understand impacts of environmental metabolism disrupting compound (MDC) exposure on both wildlife and humans. Exposure to MDCs is associated with increased risk of metabolic syndrome, including impaired lipid and glucose homeostasis, adipogenesis, appetite control, and basal metabolism. MDCs are ubiquitous in the environment, including in aquatic environments. New Bedford Harbor (NBH), Massachusetts is polluted with polychlorinated biphenyls (PCBs), and, as we show for the first time, tin (Sn). PCBs and organotins are ligands for two receptor systems known to regulate lipid homeostasis, the aryl hydrocarbon receptor (AHR) and the peroxisome proliferator-activated receptors (PPARs), respectively. In the current study, we compared lipid homeostasis in laboratory-reared killifish from NBH (F2) and a reference location (Scorton Creek, Massachusetts; F1 and F2) to evaluate how adaptation to local conditions may influence responses to MDCs. Adult killifish from each population were exposed to 3,3',4,4',5-pentachlorobiphenyl (PCB126, dioxin-like), 2,2',4,4',5,5'-hexachlorobiphenyl (PCB153, non-dioxin-like), or tributyltin (TBT, a PPARγ ligand) by a single intraperitoneal injection and analyzed after 3 days. AHR activation was assessed by measuring cyp1a mRNA expression. Lipid homeostasis was evaluated phenotypically by measuring liver triglycerides and organosomatic indices, and at the molecular level by measuring the mRNA expression of pparg and ppara and a target gene for each receptor. Acute MDC exposure did not affect phenotypic outcomes. However, overall NBH killifish had higher liver triglycerides and adiposomatic indices than SC killifish. Both season and population were significant predictors of the lipid phenotype. Acute MDC exposure altered hepatic gene expression only in male killifish from SC. PCB126 exposure induced cyp1a and pparg, whereas PCB153 exposure induced ppara. TBT exposure did not induce ppar-dependent pathways. Comparison of lipid homeostasis in two killifish populations extends our understanding of how MDCs act on fish and provides a basis to infer adaptive benefits of these differences in the wild.

Project description:Killifish survive and reproduce in the New Bedford Harbor (NBH) in Massachusetts (MA), USA, a site severely contaminated with polychlorinated biphenyls (PCBs) for decades. Levels of 22 different PCB congeners were analyzed in liver from killifish collected in 2008. Concentrations of dioxin-like PCBs in liver of NBH killifish were ∼400 times higher, and the levels of non-dioxin-like PCBs ∼3000 times higher than in killifish from a reference site, Scorton Creek (SC), MA. The NBH killifish are known to be resistant to the toxicity of dioxin-like compounds and to have a reduced aryl hydrocarbon receptor (AhR) signaling response. Little is known about the responses of these fish to non-dioxin-like PCBs, which are at extraordinarily high levels in NBH fish. In mammals, some non-dioxin-like PCB congeners act through nuclear receptor 1I2, the pregnane-X-receptor (PXR). To explore this pathway in killifish, a PXR cDNA was sequenced and its molecular phylogenetic relationship to other vertebrate PXRs was determined. Killifish were also collected in 2009 from NBH and SC, and after four months in the laboratory they were injected with a single dose of either the dioxin-like PCB 126 (an AhR agonist) or the non-dioxin-like PCB 153 (a mammalian PXR agonist). Gills and liver were sampled three days after injection and transcript levels of genes encoding PXR, cytochrome P450 3A (CYP3A), P-glycoprotein (Pgp), AhR2 and cytochrome P450 1A (CYP1A) were measured by quantitative PCR. As expected, there was little effect of PCB exposure on mRNA expression of AhR2 or CYP1A in liver and gills of NBH fish. In NBH fish, but not in SC fish, there was increased mRNA expression of hepatic PXR, CYP3A and Pgp upon exposure to either of the two PCB congeners. However, basal PXR and Pgp mRNA levels in liver of NBH fish were significantly lower than in SC fish. A different pattern was seen in gills, where there were no differences in basal mRNA expression of these genes between the two populations. In SC fish, but not in NBH fish, there was increased mRNA expression of branchial PXR and CYP3A upon exposure to PCB126 and of CYP3A upon exposure to PCB153. The results suggest a difference between the two populations in non-AhR transcription factor signaling in liver and gills, and that this could involve killifish PXR. It also implies possible cross-regulatory interactions between that factor (presumably PXR) and AhR2 in liver of these fish.

Project description:BackgroundChildren born near New Bedford, Massachusetts, have been prenatally exposed to multiple environmental chemicals, in part due to an older housing stock, maternal diet, and proximity to the New Bedford Harbor (NBH) Superfund site. Chemical exposure measures are not available for all births, limiting epidemiologic investigations and potential interventions.ObjectiveWe linked biomonitoring data from the New Bedford Cohort (NBC) and birth record data to predict prenatal exposures for all contemporaneous area births.MethodsWe used prenatal exposure biomarker data from the NBC, a population-based cohort of 788 mother-infant pairs born during 1993–1998 to mothers living near the NBH, linked to their corresponding Massachusetts birth record data, to build predictive models for cord serum polychlorinated biphenyls (expressed as a sum, [Formula: see text]), [Formula: see text] (DDE), hexachlorobenzene (HCB), cord blood lead (Pb), and maternal hair mercury (Hg). We applied the best fit models (highest pseudo [Formula: see text]), with multivariable smooths of continuous variables, to predict exposure biomarkers for all 10,270 births during 1993–1998 around the NBH. We used 10-fold cross validation to validate the exposure models and the bootstrap method to characterize sampling variability in the exposure predictions.ResultsThe 10-fold cross-validated [Formula: see text] for the [Formula: see text], DDE, HCB, Pb, and Hg exposure models were 0.54, 0.40, 0.34, 0.46, and 0.40, respectively. For each exposure model, multivariable smooths of continuous variables improved the fit compared with linear models. Other variables with significant effects on exposure estimates were paternal education, maternal race/ethnicity, and maternal ancestry. The resulting exposure predictions for all births had variability consistent with the NBC measured exposures.ConclusionsPredictive models using multivariable smoothing explained reasonable amounts of variance in prenatal exposure biomarkers. Our analyses suggest that prenatal chemical exposures can be predicted for all contemporaneous births in the same geographic area by modeling available biomarker data for a subset of that population. https://doi.org/10.1289/EHP4849.

Dataset Information

Evolutionary Toxicogenomics of the Striped Killifish (Fundulus majalis) in the New Bedford Harbor (Massachusetts, USA).

Publications

Evolutionary Toxicogenomics of the Striped Killifish (<i>Fundulus majalis</i>) in the New Bedford Harbor (Massachusetts, USA).

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