Danio rerio
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA385396 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5507580_1.fastq.gz | Fastqsanger.gz | |||
| SRR5507580_2.fastq.gz | Fastqsanger.gz | |||
| SRR5507571_1.fastq.gz | Fastqsanger.gz | |||
| SRR5507571_2.fastq.gz | Fastqsanger.gz | |||
| SRR5507581_1.fastq.gz | Fastqsanger.gz |
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Project description:In zebrafish, parental exposure to ionizing radiation has been associated with effects in offspring, such as increased DNA damage and reactive oxygen species. Here, we assessed short (one month) and long term effects (one year) on gene expression in embryonic offspring (5.5 hours post fertilization) from zebrafish exposed during gametogenesis to gamma radiation (8.7 or 53 mGy/h for 27 days, total dose 5.2 or 31 Gy). One month after exposure, a global change in gene expression was observed in offspring from the 53 mGy/h group, followed by embryonic death at late gastrula, whereas offspring from the 8.7 mGy/h group was unaffected. One year after exposure, embryos from the 8.7 mGy/h group exhibited 2455(61.8% downregulated) differentially expressed genes. Overlaps in differentially expressed genes and enriched biological pathways were evident between the 53 mGy/h group one month and 8.7 mGy/h one year after exposure, which could be linked to effects in adults and offspring, such as DNA damage and lipid peroxidation. Interestingly, pathways between the two groups were oppositely regulated. Our results indicate latent effects following ionizing radiation exposure in parents that can be transmitted to offspring and warrants monitoring effects over subsequent generations.
2017-11-05 | GSE98539 | GEO
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.
2017-12-08 | GSE100470 | GEO
Project description:Parental exposure to environmental stress factors during gestation as well as embryonal developmental may lead to deleterious consequences onto the offspring. In the present study, we assessed the adverse effects and mode of toxic action of chronic exposure to ionizing radiation over 4 generations in Caenorhabditis elegans (C. elegans). Our data show a decrease of 23% in the number of offspring on the first generation F0 and a decrease of more than 40% in subsequent generations F1, F2 and F3 from parental exposure.Transcriptomic analysis revealed modulation of a common set of genes functions betweenthrough generations that included transcription factors, as well as genes involved in stress response, unfolded protein response, lipid metabolism and reproduction. Furthermore, a drastic increase in the number of differentially expressed genes involved in defense response was measured in the last two generations, suggesting a cumulative stress effect of ionizing radiation exposure. Integration of these multi-scale data demonstrates that chronic gamma exposure can impact the germline and induce an increase in defense mechanisms, including apoptosis, antioxidant enzymes, and a modulation of lipid metabolism to improve resistance to stress. Harmful effects intensify over generations, after F0 at the phenotypic level F0 and F1 at the transcriptomic level , emphasizing the importance of studying effects of chronic exposure to pollutants over several generations.
2022-05-01 | GSE175918 | GEO
Project description:In order to investigate transcriptomic mechanisms underlying radiation exposure, we exposed zebrafish (~6 month old) to 8.7 mGy/h of g-radiation (5.2 Gy total dose) during gametogenesis for 27 days. F1 offspring from exposed parents were sampled at 5.5 hpf (late blastula/early gastrula) one year after parental exposure, for small RNA sequence analysis to determine changes in the sncRNA expression profile. Pairwise comparison between F1 generation from exposed (F1-γ), and control (F1-C) parents, revealed several classes of sncRNAs and one class of lncRNA differentially expressed. Overall, 22 miRNAs, 11 piRNA clusters, 19 snRNAs, and 21 lincRNA were found differentially expressed. When linking the DEmiRs to our previously published mRNA data, a total of 672 differentially expressed mRNAs could be linked to the DEmiRs, of which 380 followed the canonical inverse relation in miRNA-mRNA interaction. Pathway analysis revealed these 380 mRNAs involved in insulin receptor, NFkB and PTEN signaling, linking to apoptosis and cancers. The 84.2% of differentially expressed snRNAs were down-regulated in the F1-γ group, 68.8% of which were U1 and U2 snRNAs. In addition, 45% of differentially expressed DEpiRNA clusters were found associated to 9 TEs (LTR, LINE, and TIR) (p=0.0024). DEpiRNA clusters were expressed from the opposite strand of the associated TEs, indicating expression of DEpiRNAs in response to activation of TEs. Finally, 66.7% and 33.3% of lincRNAs in F1-γ were down- and up-regulated respectively. The cancer and development related lincRNAs malat-1 was found among the most down-regulated genes, denoting a link between lincRNAs expression and altered phenotypes reported previously in our parallel studies.
2021-02-09 | GSE152189 | GEO
Project description:Benzo[a]pyrene (BaP), a polycyclic aromatic hydrocarbon (PAH), is implicated in many developmental and behavioral adverse outcomes in offspring of exposed parents. Following a dietary preconceptional exposure to BaP in zebrafish, the objective of this study was to compare parental sex-dependent adverse outcomes in F1 and F2 offspring with the transcriptomic and epigenetic changes in eggs, sperm, and 10-hour post fertilization (hpf) embryos. Adult wild-type (5D) zebrafish were fed 708 µg BaP/g diet (measured) at a rate of 1% body weight twice/day (14 µg BaP/g fish/day) for 21 days. Fish were spawned using a crossover design and parental (F0) behavior and reproductive indexes measured. In offspring behavioral effects were measured at 96 hours post fertilization (hpf) in F1 & F2 larvae, and again when F1s were adult. Compared to controls, there was no significant effect of BaP exposure on adult behavior in F0, but locomotor behavior was significantly increased in F1 adults of both sexes. Larval behavior (96 hpf, photomotor response assay) was significantly altered in both the F1 and F2 generations following parental BaP exposure. To assess parental sex-dependent molecular mechanisms, BaP-mediated differential gene expression and DNA methylation changes were measured using RNAseq and RRBS, respectively, on F0 sperm and eggs and the 10 hpf embryos from all four crosses in F1 generation. Embryos resulting from the BaP male and control female cross had the most differentially methylated regions (DMRs) and differentially expressed genes. Some DMRs were associated with genes encoding chromatin modifying enzymes suggesting regulation of chromatin conformation by DNA methylation. Parental dietary BaP exposure caused persistent behavioral changes wherein the male germline contributed most significantly to the multigenerational adverse outcomes.
2022-05-26 | GSE203631 | GEO
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.
2022-10-18 | PXD031873 | Pride
Project description:We report that increased nutrient availability increases breeding success and egg production. RNA-seq analysis revealed that parental diet altered the expression of metabolic genes in the unfertilized eggs. Offspring from the differentially fed parents showed altered survival and energy expenditure as adults.
2016-11-30 | GSE81007 | GEO
Project description:Ionizing radiation, released during accidents at nuclear power plants or after atomic bomb explosions, is a potentially serious health threat for the exposed human population. This type of high-energy radiation causes DNA damage including single- and double-strand breaks and induces chromosomal rearrangements and mutations, but it is not known if ionizing radiation directly induces changes in the epigenome of irradiated cells. We treated normal human fibroblasts and normal human bronchial epithelial cells with different doses of gamma-radiation emitted from a cesium 137 (137Cs) radiation source. After a recovery period, we analyzed global DNA methylation patterns in the irradiated and control cells using the methylated-CpG island recovery assay (MIRA) method in combination with high-resolution microarrays. Bioinformatics analysis revealed only a small number of potential methylation changes with low fold-difference ratios in the irradiated cells. These minor methylation differences seen on the microarrays could not be verified by COBRA (combined bisulfite restriction analysis) or bisulfite sequencing of selected target loci. Our study shows that acute gamma-radiation treatment of two types of human cells had no appreciable effect on DNA cytosine methylation patterns in exposed cells. DNA methylation patterns in gamma-irradiated cells and non- treated cells analyzed by microarrays
2012-11-29 | E-GEOD-39038 | biostudies-arrayexpress
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2012-12-31 | E-GEOD-43206 | biostudies-arrayexpress
Project description:The goal of this study was to determine genes with altered expression after selection of ovarian cancer cells for survival in increasing concentrations of cisplatin. A series of progressively cispatin resistant derivatives of A2780 ovarian cancer cell lines was hybridized to spotted cDNA microarrays using two color technology using the parental A2780 cells as a reference. Duplicate hybridizations were carried out for each resistant derivative.
2013-12-22 | E-GEOD-44022 | biostudies-arrayexpress