Danio rerio
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA391914 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5756270_1.fastq.gz | Fastqsanger.gz | |||
| SRR5756270_2.fastq.gz | Fastqsanger.gz | |||
| SRR5756280_1.fastq.gz | Fastqsanger.gz | |||
| SRR5756280_2.fastq.gz | Fastqsanger.gz | |||
| SRR5756290_1.fastq.gz | Fastqsanger.gz |
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Project description:Ionizing radiation is known to cause DNA damage, yet the mechanisms underlying potential transgenerational effects of exposure have been scarcely studied. Previously, we observed effects in offspring of zebrafish exposed to gamma radiation during gametogenesis. Here, we hypothesize that these effects are accompanied by changes of DNA methylation possibly inherited by subsequent generations. We assessed DNA methylation in F1 embryos (5.5 hours post fertilization) with whole genome bisulfite sequencing following parental exposure to 8.7 mGy/h for 27 days and found 5658 differentially methylated regions (DMRs). DMRs were predominantly located at known regulatory regions, such as gene promoters and enhancers. Pathway analysis indicated the involvement of DMRs related to similar pathways found with gene expression analysis, such as development, apoptosis and cancers, which could be linked to previous observed developmental defects and genomic instability in the offspring. Follow up of 19 F1 DMRs in F2 and F3 embryos revealed persistent effects up to the F3 generation at 5 regions. These results indicate that ionizing radiation related effects in offspring can be linked to DNA methylation changes that partly can persist over generations. Monitoring DNA methylation could serve as a biomarker to provide an indication of ancestral exposures to ionizing radiation.
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Project description:Treatment of tumors with ionizing radiation for cancer therapy induces biological responses that include changes in cell cycle, activation of DNA repair mechanisms, and induction of apoptosis or senescence programs. What is not known is whether ionizing radiation induces an epigenetic DNA methylation response or whether epigenetic changes occur in genes in pathways classically associated with the radiation response. We exposed breast cancer cells to 0, 2, or 6 Gy and determined global DNA methylation at 1, 2, 4, 8, 24, 48, and 72 hours post-irradiation. We found that radiation treatment resulted in a DNA methylation response and that cell cycle, DNA repair, and apoptosis pathways were enriched in genes are were differentially-methylated. DNA methylation profiling of ionizing radiation treated cells using the Infinium HumanMethylation450 BeadChip.
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Project description:Methylmercury (MeHg) is a ubiquitous environmental toxicant that is often detected in the tissues of fish-eating species. It has been well established that prenatal exposure to MeHg can lead to widespread brain damage and impaired neurological development resulting in defects ranging from severe cerebral palsy and cognitive deficits to impaired motor and sensory function. A wide range of environmental toxicants have been shown to induce transgenerational inheritance of diseases via changes in DNA methylation—a well-known epigenetic modification. Our previous research has demonstrated that developmental MeHg exposure may yield transgenerational inheritance of neurological dysfunction in adult F3-lineage zebrafish via quantitative neurobehavioral assays that evaluated the visual startle response, retinal electrophysiology, and locomotor function. The objective of the current study was to examine the correlation between neurobehavioral phenotypes and the transcriptome activity in the brain and retina of F3 zebrafish by RNA sequencing (RNAseq). Transcriptomic analyses of F3 generation MeHg-treated zebrafish (compared to control) revealed significant gene dysregulation in both the brain and retina. There were 1648 and 138 differentially expressed genes in the retina and brain, respectively (FDR <0.05). Thirty-five genes were commonly dysregulated in both organs. Gene set enrichment analysis revealed significantly enriched pathways including: neurodevelopment, visual functions, phototransduction, and motor movement. Moreover, commonly dysregulated genes were associated with circadian rhythm and metabolic pathways, as well as arginine and proline metabolism. To our knowledge, this is the first evidence of a transgenerational transcriptome induced by ancestral developmental exposure to MeHg in any species. If the transgenerational phenotypes, transcriptome, homologous biomarkers, or similar molecular pathways hold true for human populations, our findings have significant impact on global public health in terms of identifying the susceptible populations using biomarkers and preventing transgenerational inheritance of MeHg-induced neurobehavioral deficits.
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Project description:Methylmercury (MeHg) is a ubiquitous environmental toxicant that is often detected in the tissues of fish-eating species. It has been well established that prenatal exposure to MeHg can lead to widespread brain damage and impaired neurological development resulting in defects ranging from severe cerebral palsy and cognitive deficits to impaired motor and sensory function. A wide range of environmental toxicants have been shown to induce transgenerational inheritance of diseases via changes in DNA methylation—a well-known epigenetic modification. Our previous research has demonstrated that developmental MeHg exposure may yield transgenerational inheritance of neurological dysfunction in adult F3-lineage zebrafish via quantitative neurobehavioral assays that evaluated the visual startle response, retinal electrophysiology, and locomotor function. The objective of the current study was to examine the correlation between neurobehavioral phenotypes and the transcriptome activity in the brain and retina of F3 zebrafish by RNA sequencing (RNAseq). Transcriptomic analyses of F3 generation MeHg-treated zebrafish (compared to control) revealed significant gene dysregulation in both the brain and retina. There were 1648 and 138 differentially expressed genes in the retina and brain, respectively (FDR <0.05). Thirty-five genes were commonly dysregulated in both organs. Gene set enrichment analysis revealed significantly enriched pathways including: neurodevelopment, visual functions, phototransduction, and motor movement. Moreover, commonly dysregulated genes were associated with circadian rhythm and metabolic pathways, as well as arginine and proline metabolism. To our knowledge, this is the first evidence of a transgenerational transcriptome induced by ancestral developmental exposure to MeHg in any species. If the transgenerational phenotypes, transcriptome, homologous biomarkers, or similar molecular pathways hold true for human populations, our findings have significant impact on global public health in terms of identifying the susceptible populations using biomarkers and preventing transgenerational inheritance of MeHg-induced neurobehavioral deficits.
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Project description:In this study, we interrogated the role of DNA methylation in HSPC generation by taking advantage of dnmt1 knockout/knockdown embryos in zebrafish. First, we generated a comprehensive DNA methylation landscape of EHT, which revealed gradually hypermethylated regions associated with vasculogenesis. Taking advantage of dnmt1-deficient embryos, we showed that the decreased DNA methylation blocked HSPC emergence. Mechanistically, we demonstrated that the decreased DNA methylation increased the expression of arterial genes and Notch signaling, thus contributing to defects in the EHT in dnmt1-deficient embryos. Herein, we identified that DNA methylation, as epigenetic regulator, participates in the negative modulation of Notch signaling through inhibiting transcription during HSPC generation in zebrafish.
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Project description:Parental exposure to environmental stress can result in an increased diseases risk in the offspring. Although literature on maternal contribution to hereditary diseases are growing, the paternal contribution is frequently underrecognized. Since human studies reported that 80% of transmitted mutations arise in the paternal germline, it is crucial to understand the mechanism underlying the paternally inherited genome instability. Ionizing radiation (IR) is a major source of mutagenesis through inducing DNA double-strand breaks (DSBs). Here, we used sex-separated C. elegans mutants to investigate the paternal contribution to IR-induced transgenerational effects. Specifically, we found that paternal exposure to IR leads to a transgenerational embryonic lethality, and this effect is only observed when the radiation exposure occurred close to the time of fertilization. In the offspring of the irradiated males (F1 generation), we detected various genome instability phenotypes, including DNA fragmentation, chromosomal rearrangement, and aneuploidy. These phenotypes are attributed to the usage of two error-prone repair machinery, the polymerase-theta mediated end joining (TMEJ) and the non-homologous End Joining (NHEJ). Surprisingly, depletion of a human histone H1.0 ortholog, HIS-24, can significantly rescue this transgenerational embryonic lethality. Moreover, this rescue effect is associated with the downregulation of heterochromatin marker histone 3 lysine 9 di-methylation (H3K9me2), and the knocking-down of heterochromatin protein, HPL-1, could mimic the rescue effect of HIS-24 depletion. We also noticed that removal of the histone H1 and heterochromatin marker could activate the error-free repair machinery, Homologous Recombination repair (HR), thus improving the viability of the offspring carrying paternally inherited DNA damage. Altogether, our work sheds light on the importance of paternal radiation exposure on the health of offspring. In addition, our work establishes a previously unknown mechanism underlying the transgenerational genome instability and provides a potential therapeutic target for preventing the hereditary diseases caused by paternal radiation exposure.
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