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  • 1
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    Development and characterization of polyclonal antibodies against the aryl hydrocarbon receptor protein family (AHR1, AHR2, and AHR repressor) of Atlantic killifish Fundulus heteroclitus (2006)
    Details
    Publication Date: 2022-05-25
    Description: Author Posting. © The Authors, 2005. This is the author's version of the work. It is posted here by permission of Elsevier B. V. for personal use, not for redistribution. The definitive version was published in Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology 142 (2006): 85-94, doi:10.1016/j.cbpc.2005.10.013.
    Description: The aryl hydrocarbon receptor (AHR) and AHR repressor (AHRR) proteins regulate gene expression in response to some halogenated aromatic hydrocarbons and polycyclic aromatic hydrocarbons. The Atlantic killifish is a valuable model of the AHR signaling pathway, but antibodies are not available to fully characterize AHR and AHRR proteins. Using bacterially expressed AHRs, we developed specific and sensitive polyclonal antisera against the killifish AHR1, AHR2, and AHRR. In immunoblots, these antibodies recognized full-length killifish AHR and AHRR proteins synthesized in rabbit reticulocyte lysate, proteins expressed in mammalian cells transfected with killifish AHR and AHRR constructs, and AHR proteins in cytosol preparations from killifish tissues. Killifish AHR1 and AHR2 proteins were detected in brain, gill, kidney, heart, liver, and spleen. Antisera specifically precipitated their respective target proteins in immunoprecipitation experiments with in vitro-expressed proteins. Killifish ARNT2 co-precipitated with AHR1 and AHR2. These sensitive, specific, and versatile antibodies will be valuable to researchers investigating AHR signaling and other physiological processes involving AHR and AHRR proteins.
    Description: Funding for this research was provided by National Institutes of Health, National Research Service Award (F32 ES05935) from the National Institute of Environmental Health Sciences (RRM), NIEHS Superfund Basic Research Program Grant P42 ES007381 at Boston University (MEH), and the Oliver S. and Jennie R. Donaldson Charitable Trust (MEH and RRM).
    Keywords: Aryl hydrocarbon receptor (AHR) ; AHR repressor (AHRR) ; Basic helix-loop-helix Per-ARNT-Sim (bHLH-PAS) ; Fish ; Halogenated aromatic hydrocarbons (HAH); ; Polynuclear aromatic hydrocarbons (PAH) ; Recombinant protein ; Teleost
    Repository Name: Woods Hole Open Access Server
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  • 2
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    Gene expression in American lobster (Homarus americanus) with epizootic shell disease (2012)
    National Shellfisheries Association
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    Publication Date: 2022-05-25
    Description: Author Posting. © National Shellfisheries Association, 2012. This article is posted here by permission of National Shellfisheries Association for personal use, not for redistribution. The definitive version was published in Journal of Shellfish Research 31 (2012): 505-513, doi:10.2983/035.031.0210.
    Description: Epizootic shell disease (ESD) has been reported widely in American lobster (Homarus americanus, Milne Edwards) in southern New England. The appearance of irregular, deep lesions—characteristic of ESD—has been associated previously with elevated levels of ecdysteroids and premature molting, but the underlying molecular and physiological changes associated with ESD remain poorly understood. Previously, we identified several genes, including arginine kinase and hemocyanin, that were expressed differentially in lobsters exhibiting signs of ESD (diseased) versus those lobsters exhibiting no signs of ESD (assumed healthy), and quantified their expression. In this study, we extend these findings and measure expression of a suite of 12 genes in tissues from 36 female lobsters of varying disease condition. In addition, molt stage is evaluated as a possible confounding factor in the expression of the selected genes. The expression of several genes changed significantly with disease stage. Arginine kinase expression decreased significantly in thoracic muscle of lobsters with signs of ESD. Ecdysteroid receptor expression was elevated significantly in both muscle and hepatopancreas of lobsters with signs of ESD. CYP45, a cytochrome P450 form that was shown previously to covary with ecdysteroid levels and to be inducible by some xenobiotics, showed significantly increased expression in hepatopancreas of lobsters with signs of ESD. Together, these results demonstrate that the expression of several genes is altered in lobsters showing signs of ESD, even when accounting for variation in molt stage. Given the observed changes in ecdysteroid receptor, arginine kinase, and CYP45 expression, further investigations of the association, if any, between molting, muscular function and xenobiotic metabolism and ESD are warranted.
    Description: This work was supported by the National Marine Fisheries Service as the New England Lobster Research Initiative: Lobster Shell Disease under NOAA grant NA06NMF4720100 to the University of Rhode Island Fisheries Center.
    Keywords: Arginine kinase ; 100 lobsters ; Cytochrome P450 ; Ecdysteroid ; Endocrine ; Hepatopancreas ; Heat shock protein ; Epizootic shell disease ; American lobster ; Shade
    Repository Name: Woods Hole Open Access Server
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  • 3
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    Teredinibacter turnerae gen. nov., sp. nov., a dinitrogen-fixing, cellulolytic, endosymbiotic c-proteobacterium isolated from the gills of wood-boring molluscs (Bivalvia: Teredinidae) (2005)
    Society for General Mircobiology
    Details
    Publication Date: 2022-05-25
    Description: Author Posting. © Society for General Mircobiology, 2002. This article is posted here by permission of Society for General Mircobiology for personal use, not for redistribution. The definitive version was published in International Journal of Systematic Bacteriology 52 (2002): 2261-2269, doi:10.1099/ijs.0.02184-0.
    Description: A cellulolytic, dinitrogen-fixing bacterium isolated from the gill tissue of a wood-boring mollusc (shipworm) Lyrodus pedicellatus of the bivalve family Teredinidae and 58 additional strains with similar properties, isolated from gills of 24 bivalve species representing 9 of 14 genera of Teredinidae, are described. The cells are Gram-negative, rigid, rods (0〈4–0〈6x3–6 lm) that bear a single polar flagellum. All isolates are capable of chemoheterotrophic growth in a simple mineral medium supplemented with cellulose as a sole source of carbon and energy. Xylan, pectin, carboxymethylcellulose, cellobiose and a variety of sugars and organic acids also support growth. Growth requires addition of combined nitrogen when cultures are vigorously aerated, but all isolates fix dinitrogen under microaerobic conditions. The pH, temperature and salinity optima for growth were determined for six isolates and are approximately 8〈5, 30–35 °C and 0〈3 M NaCl respectively. The isolates are marine. In addition to NaCl, growth requires elevated concentrations of Ca2M and Mg2M that reflect the chemistry of seawater. The DNA GMC content ranged from 49 to 51 mol%. Four isolates were identical with respect to small-subunit rRNA sequence over 891 positions compared and fall within a unique clade in the c-subclass of the Proteobacteria. Based on morphological, physiological and phylogenetic characteristics and specific symbiotic association with teredinid bivalves, a new genus and species, Teredinibacter turnerae gen. nov., sp. nov., is proposed. The type strain is T7902T (vATCC 39867TvDSM 15152T).
    Description: This work was supported by grants from the National Science Foundation no. NSF DEB-9420051 and IBN- 9982982, the Maine Science and Technology Foundation's Center for Innovation in Biotechnology, and the University of Maine's Faculty Research program.
    Keywords: Teredinidae ; Bivalvia ; Shipworms ; Symbiont ; 16S rRNA phylogeny
    Repository Name: Woods Hole Open Access Server
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  • 4
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    Identification of cinnabarinic acid as novel endogenous aryl hydrocarbon receptor ligand that drives IL-22 production (2014)
    Public Library of Science
    Details
    Publication Date: 2022-05-25
    Description: © The Author(s), 2014. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in PLoS One 9 (2014): e87877, doi:10.1371/journal.pone.0087877.
    Description: The aryl hydrocarbon receptor (AHR) binds to environmental toxicants including synthetic halogenated aromatic hydrocarbons and is involved in a diverse array of biological processes. Recently, the AHR was shown to control host immunity by affecting the balance between inflammatory T cells that produce IL-17 (Th17) and IL-22 versus regulatory T cells (Treg) involved in tolerance. While environmental AHR ligands can mediate this effect, endogenous ligands are likely to be more relevant in host immune responses. We investigated downstream metabolites of tryptophan as potential AHR ligands because (1) tryptophan metabolites have been implicated in regulating the balance between Th17 and Treg cells and (2) many of the AHR ligands identified thus far are derivatives of tryptophan. We characterized the ability of tryptophan metabolites to bind and activate the AHR and to increase IL-22 production in human T cells. We report that the tryptophan metabolite, cinnabarinic acid (CA), is an AHR ligand that stimulates the differentiation of human and mouse T cells producing IL-22. We compare the IL-22-stimulating activity of CA to that of other tryptophan metabolites and define stimulation conditions that lead to CA production from immune cells. Our findings link tryptophan metabolism to AHR activation and define a novel endogenous AHR agonist with potentially broad biological functions.
    Description: This work was supported in part by National Institutes of Health (NIH) grants OD000329 and R01AI40312 (to JMM), R01ES006272 (to MEH), P42ES007381 (Superfund Research Program at Boston University to JS, DHS and MEH), R21CA134882 (to JS), NIH Training Grant T32 GM007175 (MML), and the Harvey V. Berneking Living Trust. BK is supported by Career Development Awards from the NIH/National Institute of Diabetes and Digestive and Kidney Diseases (DK083334) and the NASPGHAN Foundation. JEM is a recipient of the Human Frontiers Science Program Long-Term Fellowship (LT000231/2011-L). JMM is a recipient of the NIH Director's Pioneer Award Program, part of the NIH Roadmap for Medical Research, through grant DPI OD00329.
    Repository Name: Woods Hole Open Access Server
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  • 5
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    Regulation of Ahr signaling by Nrf2 during development : effects of Nrf2a deficiency on PCB126 embryotoxicity in zebrafish (Danio rerio) (2015)
    Details
    Publication Date: 2022-05-25
    Description: Author Posting. © The Author(s), 2015. This is the author's version of the work. It is posted here by permission of Elsevier for personal use, not for redistribution. The definitive version was published in Aquatic Toxicology 167 (2015): 157-171, doi:10.1016/j.aquatox.2015.08.002.
    Description: The embryotoxicity of co-planar PCBs is regulated by the aryl hydrocarbon receptor (Ahr), and has been reported to involve oxidative stress. Ahr participates in crosstalk with another transcription factor, Nfe2l2, or Nrf2. Nrf2 binds to antioxidant response elements to regulate the adaptive response to oxidative stress. To explore aspects of the crosstalk between Nrf2 and Ahr and its impact on development, we used zebrafish (Danio rerio) with a mutated DNA binding domain in Nrf2a (nrf2afh318/fh318), rendering these embryos more sensitive to oxidative stress. Embryos were exposed to 2 nM or 5 nM PCB126 at 24 hours post fertilization (prim-5 stage of pharyngula) and examined for gene expression and morphology at 4 days post fertilization (dpf; protruding –mouth stage). Nrf2a mutant eleutheroembryos were more sensitive to PCB126 toxicity at 4 dpf, and in the absence of treatment also displayed some subtle developmental differences from wildtype embryos, including delayed inflation of the swim bladder and smaller yolk sacs. We used qPCR to measure changes in expression of the nrf gene family, keap1a, keap1b, the ahr gene family, and known target genes. cyp1a induction by PCB126 was enhanced in the Nrf2a mutants (156-fold in wildtypes vs. 228-fold in mutants exposed to 5 nM). Decreased expression of heme oxygenase (decycling) 1 (hmox1) in the Nrf2a mutants was accompanied by increased nrf2b expression. Target genes of Nrf2a and AhR2, NAD(P)H:quinone oxidoreductase 1 (nqo1) and glutathione S-transferase, alpha-like (gsta1), showed a 2-5-fold increase in expression in the Nrf2a mutants as compared to wildtype. This study elucidates the interaction between two important transcription factor pathways in the developmental toxicity of co-planar PCBs.
    Description: University of Massachusetts Amherst Commonwealth Honors College Research grant (to M.R.), National Institutes of Health grants R01ES016366 (MEH), R01ES006272 (MEH), and F32ES017585 (ART-L).
    Keywords: Transcription factor ; Dioxin-like compound ; Gene expression ; Embryonic development ; Swim bladder ; Yolk
    Repository Name: Woods Hole Open Access Server
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  • 6
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    The molecular basis for differential dioxin sensitivity in birds : role of the aryl hydrocarbon receptor (2006)
    National Academy of Sciences
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    Publication Date: 2022-05-25
    Description: Author Posting. © National Academy of Sciences, 2006. This article is posted here by permission of National Academy of Sciences for personal use, not for redistribution. The definitive version was published in Proceedings of the National Academy of Sciences 103 (2006): 6252-6257, doi:10.1073/pnas.0509950103.
    Description: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related halogenated aromatic hydrocarbons (HAHs) are highly toxic to most vertebrate animals, but there are dramatic differences in sensitivity among species and strains. Aquatic birds including the common tern (Sterna hirundo) are highly exposed to HAHs in the environment, but are up to 250-fold less sensitive to these compounds than the typical avian model, the domestic chicken (Gallus gallus). The mechanism of HAH toxicity involves altered gene expression subsequent to activation of the aryl hydrocarbon receptor (AHR), a basic helix–loop–helix-PAS transcription factor. AHR polymorphisms underlie mouse strain differences in sensitivity to HAHs and polynuclear aromatic hydrocarbons, but the role of the AHR in species differences in HAH sensitivity is not well understood. Here, we show that although chicken and tern AHRs both exhibit specific binding of [3H]TCDD, the tern AHR has a lower binding affinity and exhibits a reduced ability to support TCDD-dependent transactivation as compared to AHRs from chicken or mouse. We further show through use of chimeric AHR proteins and site-directed mutagenesis that the difference between the chicken and tern AHRs resides in the ligand-binding domain and that two amino acids (Val-325 and Ala-381) are responsible for the reduced activity of the tern AHR. Other avian species with reduced sensitivity to HAHs also possess these residues. These studies provide a molecular understanding of species differences in sensitivity to dioxin-like compounds and suggest an approach to using the AHR as a marker of dioxin susceptibility in wildlife.
    Description: This research was supported by the National Oceanographic and Atmospheric Administration National Sea Grant College Program, Department of Commerce, under Grants NA46RG0470 and NA16RG2273.
    Keywords: Basic helix–loop–helix-PAS ; Comparative toxicology ; Mechanisms ; Risk assessment ; Susceptibility
    Repository Name: Woods Hole Open Access Server
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  • 7
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    Genetic variation at aryl hydrocarbon receptor (AHR) loci in populations of Atlantic killifish (Fundulus heteroclitus) inhabiting polluted and reference habitats (2014)
    BioMed Central
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    Publication Date: 2022-05-26
    Description: © The Author(s), 2014. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in BMC Evolutionary Biology 14 (2014): 6, doi:10.1186/1471-2148-14-6.
    Description: The non-migratory killifish Fundulus heteroclitus inhabits clean and polluted environments interspersed throughout its range along the Atlantic coast of North America. Several populations of this species have successfully adapted to environments contaminated with toxic aromatic hydrocarbon pollutants such as polychlorinated biphenyls (PCBs). Previous studies suggest that the mechanism of resistance to these and other “dioxin-like compounds” (DLCs) may involve reduced signaling through the aryl hydrocarbon receptor (AHR) pathway. Here we investigated gene diversity and evidence for positive selection at three AHR-related loci (AHR1, AHR2, AHRR) in F. heteroclitus by comparing alleles from seven locations ranging over 600 km along the northeastern US, including extremely polluted and reference estuaries, with a focus on New Bedford Harbor (MA, USA), a PCB Superfund site, and nearby reference sites. We identified 98 single nucleotide polymorphisms within three AHR-related loci among all populations, including synonymous and nonsynonymous substitutions. Haplotype distributions were spatially segregated and F-statistics suggested strong population genetic structure at these loci, consistent with previous studies showing strong population genetic structure at other F. heteroclitus loci. Genetic diversity at these three loci was not significantly different in contaminated sites as compared to reference sites. However, for AHR2 the New Bedford Harbor population had significant FST values in comparison to the nearest reference populations. Tests for positive selection revealed ten nonsynonymous polymorphisms in AHR1 and four in AHR2. Four nonsynonymous SNPs in AHR1 and three in AHR2 showed large differences in base frequency between New Bedford Harbor and its reference site. Tests for isolation-by-distance revealed evidence for non-neutral change at the AHR2 locus. Together, these data suggest that F. heteroclitus populations in reference and polluted sites have similar genetic diversity, providing no evidence for strong genetic bottlenecks for populations in polluted locations. However, the data provide evidence for genetic differentiation among sites, selection at specific nucleotides in AHR1 and AHR2, and specific AHR2 SNPs and haplotypes that are associated with the PCB-resistant phenotype in the New Bedford Harbor population. The results suggest that AHRs, and especially AHR2, may be important, recurring targets for selection in local adaptation to dioxin-like aromatic hydrocarbon contaminants.
    Description: This work was supported in part by the Hudson River Foundation (grant 004/02A; final report available at http://www.hudsonriver.org/ls/), by National Institute of Environmental Health Sciences (NIEHS) grant P42ES007381 (Superfund Basic Research Program at Boston University), by grant F32HD062178 from the Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHHD), and by the National Science Foundation (DEB-1120263). Data interpretation was aided by reference to a preliminary draft of the F. heteroclitus genome sequence, which was supported by funding from the National Science Foundation (collaborative research grants DEB-1120512, DEB-1265282, DEB-1120013, DEB-1120263, DEB-1120333, DEB-1120398).
    Keywords: Local adaptation ; Pollution ; Molecular mechanism ; Resistance ; Tolerance ; Convergent evolution ; Population genetics
    Repository Name: Woods Hole Open Access Server
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  • 8
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    Transcriptomic assessment of resistance to effects of an aryl hydrocarbon receptor (AHR) agonist in embryos of Atlantic killifish (Fundulus heteroclitus) from a marine Superfund site (2011)
    BioMed Central
    Details
    Publication Date: 2022-05-26
    Description: © The Author(s), 2011. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in BMC Genomics 12 (2011): 263, doi:10.1186/1471-2164-12-263.
    Description: Populations of Atlantic killifish (Fundulus heteroclitus) have evolved resistance to the embryotoxic effects of polychlorinated biphenyls (PCBs) and other halogenated and nonhalogenated aromatic hydrocarbons that act through an aryl hydrocarbon receptor (AHR)-dependent signaling pathway. The resistance is accompanied by reduced sensitivity to induction of cytochrome P450 1A (CYP1A), a widely used biomarker of aromatic hydrocarbon exposure and effect, but whether the reduced sensitivity is specific to CYP1A or reflects a genome-wide reduction in responsiveness to all AHR-mediated changes in gene expression is unknown. We compared gene expression profiles and the response to 3,3',4,4',5-pentachlorobiphenyl (PCB-126) exposure in embryos (5 and 10 dpf) and larvae (15 dpf) from F. heteroclitus populations inhabiting the New Bedford Harbor, Massachusetts (NBH) Superfund site (PCB-resistant) and a reference site, Scorton Creek, Massachusetts (SC; PCB-sensitive). Analysis using a 7,000-gene cDNA array revealed striking differences in responsiveness to PCB-126 between the populations; the differences occur at all three stages examined. There was a sizeable set of PCB-responsive genes in the sensitive SC population, a much smaller set of PCB-responsive genes in NBH fish, and few similarities in PCB-responsive genes between the two populations. Most of the array results were confirmed, and additional PCB-regulated genes identified, by RNA-Seq (deep pyrosequencing). The results suggest that NBH fish possess a gene regulatory defect that is not specific to one target gene such as CYP1A but rather lies in a regulatory pathway that controls the transcriptional response of multiple genes to PCB exposure. The results are consistent with genome-wide disruption of AHR-dependent signaling in NBH fish.
    Description: This work was supported in part by National Institutes of Health grants P42ES007381 (Superfund Basic Research Program at Boston University) and by a grant from the WHOI Ocean Life Institute.
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  • 9
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    The transcriptional response to oxidative stress during vertebrate development : effects of tert-butylhydroquinone and 2,3,7,8-tetrachlorodibenzo-p-dioxin (2014)
    Public Library of Science
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    Publication Date: 2022-05-26
    Description: © The Author(s), 2014. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in PLoS One 9 (2014): e113158, doi:10.1371/journal.pone.0113158.
    Description: Oxidative stress is an important mechanism of chemical toxicity, contributing to teratogenesis and to cardiovascular and neurodegenerative diseases. Developing animals may be especially sensitive to chemicals causing oxidative stress. The developmental expression and inducibility of anti-oxidant defenses through activation of NF-E2-related factor 2 (NRF2) affect susceptibility to oxidants, but the embryonic response to oxidants is not well understood. To assess the response to chemically mediated oxidative stress and how it may vary during development, zebrafish embryos, eleutheroembryos, or larvae at 1, 2, 3, 4, 5, and 6 days post fertilization (dpf) were exposed to DMSO (0.1%), tert-butylhydroquinone (tBHQ; 10 µM) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; 2 nM) for 6 hr. Transcript abundance was assessed by real-time qRT-PCR and microarray. qRT-PCR showed strong (4- to 5-fold) induction of gstp1 by tBHQ as early as 1 dpf. tBHQ also induced gclc (2 dpf), but not sod1, nqo1, or cyp1a. TCDD induced cyp1a but none of the other genes. Microarray analysis showed that 1477 probes were significantly different among the DMSO-, tBHQ-, and TCDD-treated eleutheroembryos at 4 dpf. There was substantial overlap between genes induced in developing zebrafish and a set of marker genes induced by oxidative stress in mammals. Genes induced by tBHQ in 4-dpf zebrafish included those involved in glutathione synthesis and utilization, signal transduction, and DNA damage/stress response. The strong induction of hsp70 determined by microarray was confirmed by qRT-PCR and by use of transgenic zebrafish expressing enhanced green fluorescent protein (EGFP) under control of the hsp70 promoter. Genes strongly down-regulated by tBHQ included mitfa, providing a molecular explanation for the loss of pigmentation in tBHQ-exposed embryos. These data show that zebrafish embryos are responsive to oxidative stress as early as 1 dpf, that responsiveness varies with development in a gene-specific manner, and that the oxidative stress response is substantially conserved in vertebrate animals.
    Description: This research was supported in part by National Institutes of Health grants R01ES016366 (MEH), R01ES006272 (MEH), R01ES015912 (JJS), and F32ES017585 (ART-L), the Andrew W. Mellon Foundation Endowed Fund for Innovative Research, a WHOI (Woods Hole Oceanographic Institution) Postdoctoral Scholar award, and the Walter A. and Hope Noyes Smith endowed chair (MEH). AGM and MJC were supported in part by the Marine Biological Laboratory's Program in Global Infectious Disease, funded by the Ellison Medical Foundation.
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