Transgenerational whole genome bisulphite sequencing data from adult zebrafish exposed to low level TCDD
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA630486 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11692105_1.fastq.gz | Fastqsanger.gz | |||
| SRR11692105_2.fastq.gz | Fastqsanger.gz | |||
| SRR11692106_1.fastq.gz | Fastqsanger.gz | |||
| SRR11692106_2.fastq.gz | Fastqsanger.gz | |||
| SRR11692107_1.fastq.gz | Fastqsanger.gz |
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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 WGBS to investigate differential methylation in testicular tissue and identified distinct multigenerational and transgenerational methylation changes due to legacy TCDD exposure in males.
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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.
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Project description:Transgenerational expression data from adult zebrafish exposed to low level TCDD
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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.
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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.
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2014-03-01 | E-MTAB-2057 | biostudies-arrayexpress
Project description:Juvenile zebrafish were fed Biodiet starter (4% body weight per day) for 42 d with TCDD added at 0 ppb, 0.1 ppb, 1 ppb, 10 ppb or 100 ppb. Fish were collected, sexed, weighed and length measured at 0, 7, 14, 28 or 42 d for TCDD assessment, histopathologic and microarray analysis. Microarray experiments were conducted in TCDD-treated (at 0, 0.1, 1, 10 and 100 ppb) for male and female sexed zebrafish at 28 d. NimbleGen Gene Expression 12X135K zebrafish microarrays and One-Color DNA labeling Kit (NimbleGen, WI) were used for genome-wide expression analysis of TCDD-treated zebrafish. TCDD accumulated in a dose- and time-dependent manner and 100 ppb TCDD caused TCDD accumulation in female (15.49 ppb) and male (18.04 ppb) fish at 28 d post exposure. TCDD caused multiple lesions in liver, kidney, intestine and ovary of zebrafish and functional dysregulation such as depletion of glycogen in liver, retrobulbar edema, degeneration of neurosensory epithelium, underdevelopment of intestine, and diminution in the fraction of ovarian follicles containing vitellogenic oocytes. Microarray gene expression analysis comparing control to post TCDD diet revealed dysregulated genes located in pathways associated with cardiac necrosis/cell death, cardiac fibrosis, renal necrosis/cell death and liver necrosis/cell death. These baseline toxicological effects provide evidence for the potential biomarkers, mechanisms and pathology of TCDD induced dysregulation.
2014-12-01 | GSE47434 | GEO
Project description:Juvenile zebrafish were fed Biodiet starter (4% body weight per day) for 42 d with TCDD added at 0 ppb, 0.1 ppb, 1 ppb, 10 ppb or 100 ppb. Fish were collected, sexed, weighed and length measured at 0, 7, 14, 28 or 42 d for TCDD assessment, histopathologic and microarray analysis. Microarray experiments were conducted using 0 and 100 ppb-TCDD treated male and female sexed zebrafish at 7, 14, 28 and 42 d. NimbleGen Gene Expression 12X135K zebrafish microarrays and One-Color DNA labeling Kit (NimbleGen, WI) were used for genome-wide expression analysis of TCDD-treated zebrafish. TCDD accumulated in a dose- and time-dependent manner and 100 ppb TCDD caused TCDD accumulation in female (15.49 ppb) and male (18.04 ppb) fish at 28 d post exposure. TCDD caused multiple lesions in liver, kidney, intestine and ovary of zebrafish and functional dysregulation such as depletion of glycogen in liver, retrobulbar edema, degeneration of neurosensory epithelium, underdevelopment of intestine, and diminution in the fraction of ovarian follicles containing vitellogenic oocytes. At 42d, no mature female fish were observed.
2014-12-01 | GSE47547 | GEO
Project description:The legacy endocrine disrupting chemical and aryl hydrocarbon receptor agonist, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), is produced as a byproduct of industrial processes and causes adverse health effects ranging from skin irritation to cancer. TCDD endpoints are also observed in subsequent, unexposed generations; however, the mechanisms of these multi- and transgenerational effects are unknown. We hypothesized an epigenetic mechanism, specifically DNA methylation for the transgenerational, male-mediated reproductive effects of developmental TCDD exposure. Using whole genome bisulfite sequencing, we evaluated DNA methylation changes in three generations of zebrafish, the first of which was exposed to TCDD during sexual development at 50 ppt for 1 h at both 3- and 7-week post-fertilization. We discovered that TCDD induces multi- and transgenerational methylomic changes in testicular tissue from zebrafish with decreased reproductive capacity, but most significantly in the indirectly exposed F1 generation. In comparing differentially methylated genes to concurrent transcriptomic changes, we identified several genes and pathways through which transgenerational effects of low level TCDD exposure are likely inherited. These include significant differential methylation of genes involved in reproduction, endocrine function, xenobiotic metabolism, and epigenetic processing. Notably, a number of histone modification genes were both differentially methylated and expressed in all generations, and many differentially methylated genes overlapped between multiple generations. Collectively, our results suggest that DNA methylation is a promising mechanism to explain male-mediated transgenerational reproductive effects of TCDD exposure in zebrafish, and these effects are likely inherited through integration of multiple epigenetic pathways.
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