Project description:Atrazine is an agricultural herbicide used throughout the Midwestern United States that frequently contaminates potable water supplies resulting in human exposure. Using the zebrafish model system, an embryonic atrazine exposure was previously reported to decrease spawning rates with an increase in progesterone and ovarian follicular atresia in adult females. In addition, alterations in genes associated with distinct molecular pathways of the endocrine system were observed in brain and gonad tissue of the adult females and males. Current hypotheses for mechanistic changes in the developmental origins of health and disease include genetic (e.g., copy number alterations) or epigenetic (e.g., DNA methylation) mechanisms. As such, in the current study we investigated whether an atrazine exposure would generate copy number alterations (CNAs) in the zebrafish genome. A zebrafish fibroblast cell line was used to limit detection to CNAs caused by the chemical exposure. First, cells were exposed to a range of atrazine concentrations and a crystal violet assay was completed, showing confluency decreased by ~60% at 46.3 µM. Cells were then exposed to 0, 0.463, 4.63, or 46.3 µM atrazine and array comparative genomic hybridization completed. Results showed 34, 21, and 44 CNAs in the 0.463, 4.63, and 46.3µM treatments, respectively. Furthermore, CNAs were associated with previously reported gene expression alterations in adult male and female zebrafish. This study demonstrates that atrazine exposure can generate CNAs that are linked to gene expression alterations observed in adult zebrafish exposed to atrazine during embryogenesis providing a mechanism of the developmental origins of atrazine endocrine disruption.
2017-02-20 | GSE93635 | GEO
Project description:Microbial community for atrazine degradation with virus infection (Metagenome)
Project description:In this study, two multiantibiotic-resistant bacteria, Ochrobactrum intermedium (N1) and Stenotrophomonas acidaminiphila (N2), were isolated from the sludge of a PWWTP in Guangzhou, China. Whole-genome sequencing revealed that N1 and N2 had genome sizes of 0.52 Mb and 0.37 Mb, respectively, and harbored 33 and 24 ARGs, respectively. The main resistance mechanism in the identified ARGs included efflux pumps, enzymatic degradation, and target bypass, with the N1 strain possessing more multidrug-resistant efflux pumps than the N2 strain (22 vs 12). This also accounts for the broader resistance spectrum of N1 than of N2 in antimicrobial susceptibility tests. Additionally, both genomes contain numerous mobile genetic elements (89 and 21 genes, respectively) and virulence factors (276 and 250 factors, respectively), suggesting their potential for horizontal transfer and pathogenicity.
Project description:Large amounts of carbon sequestered in permafrost are becoming available for microbial degradation. We investigated 1,529 microbial metagenome-assembled genomes recovered from our site to understand carbon processing in this environment. Metabolic reconstruction, supported by metatranscriptomic and metaproteomic data, revealed key populations involved in organic matter degradation, including bacteria encoding a pathway for xylose degradation only previously identified in fungi.
Project description:Atrazine, a herbicide commonly applied to agricultural areas and a common contaminant of potable water supplies, is implicated as an endocrine-disrupting chemical (EDC) and potential carcinogen. Studies show that EDCs can cause irreversible changes in tissue formation, decreased reproductive potential, obesity, and cancer. The U.S. Environmental Protection Agency considers an atrazine concentration of ≤ 3 ppb in drinking water safe for consumption. The specific adverse human health effects associated with a developmental atrazine exposure and the underlying genetic mechanisms of these effects are not well defined. In this study, zebrafish embryos were exposed to a range of atrazine concentrations to establish toxicity. Morphological, transcriptomic, and protein alterations were then assessed at 72 h postfertilization following developmental atrazine exposure at 0, 0.3, 3, or 30 ppb. A significant increase in head length was observed in all three atrazine treatments. Transcriptomic profiles revealed 21, 62, and 64 genes with altered expression in the 0.3, 3, and 30 ppb atrazine treatments, respectively. Altered genes were associated with neuroendocrine and reproductive system development, function, and disease; cell cycle control; and carcinogenesis. There was a significant overlap (42 genes) between the 3 and 30 ppb differentially expressed gene lists, with two of these genes (CYP17A1 and SAMHD1) present in all three atrazine treatments. Increased transcript levels were translated to significant upregulation in protein expression. Overall, this study identifies genetic and molecular targets altered in response to a developmental atrazine exposure to further define the biological pathways and mechanisms of toxicity.
Project description:The aquatic midge, Chironomus tentans, is a keystone species in aquatic ecosystem and used as a model organism to assess chemicals toxicity in aquatic environment. To characterize midge’s cellular and molecular responses to pesticides, we established cDNA library with 10,000 cDNA elements representing 2,456 C. tentans unique genes. Blast2go identified 49 genes potentially involved in xenobiotics metabolism, including 24 cytochrome p450s (CYPs), 14 esterases (ESTs) and 11 glutathione-s-transferases (GSTs). Based on 2,456 unique genes, a cDNA microarray was developed to monitor gene expression profiles in 4th instar larvae under chlopyrifos (0.1 µg/L and 0.5 µg/L) and 1000 µg/L atrazine 48-hr exposure. We identified 149, 435 and 244 genes were significantly differentially expressed (p-value ≤0.05 with expression ratios ≥2.0) after 0.1 µg/L, 0.5 µg/L chlopyrifos, and 1000 µg/L atrazine application, respectively. Sixteen insect detoxification genes (11 CYPs, 3 GSTs and 2 esterases) were validated by qPCR and their expressions were significantly either up- or down-regulated under chlorpyrifos and atrazine exposure, especially the expression of 10 CYPs were significantly induced after chlopyrifos and atrazine exposure. The up-regulated CYPs might be involved in xenobiotic activation and/or degradation. Furthermore, we also found 5 differentially expressed hemoglobin genes. The expression changes of hemoglobins might be an adaption mechanism of C. tentans to hypoxic condition caused by xenobiotic exposure. This study provides a platform for further functional studies of pesticide-insect interactions in C. tentans.
Project description:The study of epigenetic mechanisms of gene regulation and the role of these mechanisms in developmental reprogramming of the genome and disease susceptibility has increased in recent years. Molecular epigenetic mechanisms regulating gene expression include DNA methylation, histone modifications, and small non-coding RNAs (e.g., microRNAs). MicroRNAs (miRNAs) are short, single-stranded RNA that regulate post-transcriptional control of the translation of mRNA. The importance of these epigenetic regulators in controlling developmental processes is becoming clear. However, to date, few studies have investigated the role of miRNAs in toxicological responses limiting knowledge of these critical regulators in mechanisms of toxicity. Atrazine is a herbicide commonly used throughout the Midwestern United States and other areas of the globe for control of weeds in agricultural crops. In certain areas of the United States, atrazine frequently contaminates potable water supplies above the maximum contaminant level of 3 parts per billion (ppb; mg/L) as set by the United States Environmental Protection Agency (U.S. EPA) and is a suspected endocrine disrupting chemical. Studies have begun to investigate the genetic mechanisms of atrazine toxicity; however, studies investigating epigenetic mechanisms are limited. Here we report that expression of both zebrafish and human miRNAs are significantly altered in response to a developmental atrazine exposure of 0.3, 3, or 30 ppb from 1-72 hours post fertilization (hpf). Altered miRNAs are known to play a role in angiogenesis, cancer, or neuronal development, differentiation, and maturation. Targeted analysis of altered human miRNAs with genes previously identified to be altered by atrazine exposure revealed several targets linked to cell cycle and cell signaling. Further analysis of hsa-miRNA-126-3p which had altered expression in all three atrazine treatments at 72 hpf revealed alterations also occurred at 60 hpf in the 30 ppb treatment group. Results from this study indicate miRNA deregulation in zebrafish and human miRNAs following an embryonic atrazine exposure in zebrafish.