Transgenerational expression data from adult zebrafish exposed to low level TCDD
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PROVIDER: PRJNA437066 | ENA |
REPOSITORIES: ENA
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Project description:Exposure to TCDD early in development produces reproductive abnormalities and decreased reproductive capacity in males in subsequent generations We used microarrays to investigate the global programme of gene expression in testicular tissue and identified distinct multigenerational and transgenerational gene expression changes due to legacy TCDD exposure in males.
2018-10-01 | GSE111446 | GEO
Project description:Exposure to TCDD early in development produces reproductive abnormalities and decreased reproductive capacity in males in subsequent generations. We used WGBS to investigate differential methylation in testicular tissue and identified distinct multigenerational and transgenerational methylation changes due to legacy TCDD exposure in males.
2022-04-20 | GSE149919 | GEO
Project description:Transgenerational whole genome bisulphite sequencing data from adult zebrafish exposed to low level TCDD
| PRJNA630486 | ENA
Project description:Exposure to TCDD early in development produces reproductive abnormalities in adulthood and decreased reproductive capacity in males We used microarrays to investigate the global programme of gene expression in testicular tissue and identified distinct gene expression changes due to TCDD exposure in males.
2016-09-30 | GSE77335 | GEO
Project description:Environmental compounds can promote epigenetic transgenerational inheritance of adult-onset disease in subsequent generations following ancestral exposure during fetal gonadal sex determination. The current study examined the ability of dioxin (2,3,7,8-tetrachlorodibenzo[p]dioxin, TCDD) to promote epigenetic transgenerational inheritance of disease and DNA methylation epimutations in sperm. Gestating F0 generation females were exposed to dioxin during fetal day 8 to 14 and adult-onset disease was evaluated in F1 and F3 generation rats. The incidences of total disease and multiple disease increased in F1 and F3 generations. Prostate disease, ovarian primordial follicle loss and polycystic ovary disease were increased in F1 generation dioxin lineage. Kidney disease in males, pubertal abnormalities in females, ovarian primordial follicle loss and polycystic ovary disease were increased in F3 generation dioxin lineage animals. Analysis of the F3 generation sperm epigenome identified 50 differentially DNA methylated regions (DMR) in gene promoters. These DMR provide potential epigenetic biomarkers for transgenerational disease and ancestral environmental exposures. Observations demonstrate dioxin exposure of a gestating female promotes epigenetic transgenerational inheritance of adult onset disease and sperm epimutations. Methylated sperm DNA was isolated from rats ancestrally exposed to dioxin (Hip). Three independent samples from the treatment group were obtained. Differential DNA methylation between treatment groups was determined using Nimblegen microarrays. Treated samples were paired with control samples and hybridized together on arrays (Hip1/Cip1, Hip2/Cip2, and Hip3/Cip3), resulting in three arrays for the treatment.
2014-07-22 | E-GEOD-59552 | biostudies-arrayexpress
Project description:Environmental compounds can promote epigenetic transgenerational inheritance of adult-onset disease in subsequent generations following ancestral exposure during fetal gonadal sex determination. The current study examined the ability of dioxin (2,3,7,8-tetrachlorodibenzo[p]dioxin, TCDD) to promote epigenetic transgenerational inheritance of disease and DNA methylation epimutations in sperm. Gestating F0 generation females were exposed to dioxin during fetal day 8 to 14 and adult-onset disease was evaluated in F1 and F3 generation rats. The incidences of total disease and multiple disease increased in F1 and F3 generations. Prostate disease, ovarian primordial follicle loss and polycystic ovary disease were increased in F1 generation dioxin lineage. Kidney disease in males, pubertal abnormalities in females, ovarian primordial follicle loss and polycystic ovary disease were increased in F3 generation dioxin lineage animals. Analysis of the F3 generation sperm epigenome identified 50 differentially DNA methylated regions (DMR) in gene promoters. These DMR provide potential epigenetic biomarkers for transgenerational disease and ancestral environmental exposures. Observations demonstrate dioxin exposure of a gestating female promotes epigenetic transgenerational inheritance of adult onset disease and sperm epimutations.
2014-07-22 | GSE59552 | GEO
Project description:Exposure to environmental contaminants can disrupt normal development of the early vertebrate skeleton. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) impairs craniofacial skeletal development across many vertebrate species and its effects are especially prominent in early life stages of fish. TCDD activates the aryl hydrocarbon receptor (AHR), a transcription factor that mediates most if not all TCDD responses. We investigated the transcriptional response in the developing zebrafish jaw following TCDD exposure using DNA microarrays. Zebrafish larvae were exposed to TCDD at 96 h postfertilization (hpf) and jaw cartilage tissue was harvested for microarray analysis at 1, 2, 4 and 12 h postexposure (hpe). Numerous chondrogenic transcripts were misregulated by TCDD in the jaw. Comparison of transcripts altered by TCDD in jaw with transcripts altered in embryonic heart showed that the transcriptional responses in the jaw and the heart were strikingly different. Sox9b, a critical chondrogenic transcription factor, was the most significantly reduced transcript in the jaw. We hypothesized that the TCDD reduction of sox9b expression plays an integral role in affecting formation of the embryonic jaw. Morpholino knock down of sox9b expression demonstrated that partial reduction of sox9b expression alone was sufficient to produce a TCDD-like jaw phenotype. Heterozygous sox9b deletion mutant embryos were sensitized to TCDD. Lastly, embryos injected with sox9b mRNA and then exposed to TCDD blocked TCDD-induced jaw toxicity in approximately 14% of sox9b-injected embryos. These results suggest that reduced sox9b expression in TCDD-exposed zebrafish embryos contributes to jaw malformation. Keywords: Time course
2008-11-01 | GSE11893 | GEO
Project description:To fully understand molecular toxicity of TCDD in an in vivo animal model, adult zebrafish were exposed to TCDD at 10 nM for 96 h and the livers were sampled for RNA-sequencing based transcriptomic profiling. A total of 1,058 differently expressed genes were identified based on fold-change>2 and TPM (transcripts per million) >10. Among the top 20 up-regulated genes, 10 novel responsive genes were identified and verified by qRT-PCR analysis on independent samples. Transcriptomic analysis indicated several deregulated pathways associated with cell cycle, endocrine disruptors, signal transduction and immune systems. Comparative analyses of TCDD-induced transcriptomic changes between fish and mammalian models revealed that proteomic pathway is consistently up-regulated while calcium signaling pathway and several immune-related pathways are generally down-regulated.
2013-11-12 | GSE49915 | GEO
Project description:2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a persistent environmental contaminant. Previous reports revealed TCDD activating aryl hydrocarbon receptor (AhR) pathway and causing cardiac damage. However, the mechanism of AhR-induced cardiac defect in response to TCDD exposure remains unclear. In this study, we characterized the impacts of TCDD exposure on heart morphology and cardiac function in zebrafish. To investigate the differentially expressed genes under TCDD exposure, we collected the zebrafish larave heart from the control and TCDD treatment groups. We then performed gene expression profiling analysis using data obtained from RNA-seq. Transcriptomic profiling showed that, along with an upregulation of the AhR signaling pathway by TCDD, the expression of pro-ferroptosis genes was upregulated, while genes implicated in glutathione metabolism were downregulated. Consistently, lipid peroxidation, as indicated by malonaldehyde (MDA) production, increased in TCDD-exposed cardiac tissue. Accordingly, inhibiting lipid peroxidation with Liproxstatin-1 reversed the adverse cardiac effects under TCDD treatment. Together, our findings demonstrate that AhR-mediated lipid peroxidation contributes to the cardiac developmental defects of TCDD during zebrafish early development.
2022-10-30 | GSE206948 | GEO
Project description:This experiment investigates the role of a novel AHR-regulated gene on the global transcriptome in 48 hpf zebrafish exposed to 0.1% DMSO or 1 ng/mL TCDD.
2021-04-21 | GSE172418 | GEO