Transgenerational effects of paternal restraint stress in Drosophila
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ABSTRACT:
PROVIDER: PRJNA591569 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10529200.fastq.gz | Fastqsanger.gz | |||
| SRR10529201.fastq.gz | Fastqsanger.gz | |||
| SRR10529202.fastq.gz | Fastqsanger.gz | |||
| SRR10529203.fastq.gz | Fastqsanger.gz | |||
| SRR10529204.fastq.gz | Fastqsanger.gz |
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Project description:At present, the experimental evidences of epigenetic inheritance caused by stresses are beginning to accumulate in some animal models. However, molecular mechanism and biological meaning underlying these phenomena has not been clearly understood yet. Previously, we showed that Drosophila transcription factor-2 (dATF-2) is involved in heterochromatin formation and that phosphorylation of dATF-2 by various stresses, such as heat shock and osmotic stresses, induces heterochromatin disruption. We also revealed these stress dependent epigenome changes mediated by dATF-2 can be inherited to next generations (Seong et al., 2011). In this study, we established a drosophila model of restraint stress (RS) to analyze the transgenerational effects of strong psychological stress. We observed that Drosophila F1 progenies, derived from RS exposed fathers, showed significant disruption of heterochromatin state and that such effect was not observed in the dATF-2 and MEKK1 mutant background. To reveal trangenerational effects and role of paternal restraint stress, we analyzed gene expression profiles of F1 progenies derived from either RS exposed or control fathers of wild-type and dATF-2 KO father.
2020-04-29 | GSE140950 | 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:Purpose: Paternal life experiences impact offspring health via germline, and epigenetic inheritance provides a potential mechanism. However, global reprogramming during offspring embryogenesis and gametogenesis represents the largest hurdle to conceptualize it. Yet, detailed characterization of how sperm epigenetic alterations carrying “environmental memory” can evade offspring embryonic reprogramming remains elusive. Methods: we profiled the sperm DNA methylation patterns of three consecutive generations (F0, F1 and F2) in both control and stress groups by using whole-genome bisulfite sequencing (WGBS). A total of 18 sperm samples were analyzed, including three biological replicates for each generation under each treatment. In addition, small RNA sequencing was carried out on paternal sperm samples to investigate whether long-term psychological stress affected the enrichment of certain sncRNAs and to identify whether they participated in mediating the occurrence and paternal inheritance of the stress-induced DMRs Rsults: Using an optimized data analysis workflow, we obtained approximately 800 million clean reads per sample (build mm10) with strand-specific coverage ~21×, and the data covered ~96.00% of the total 21,867,837 reference CpG dinucleotides. A total of 24,427, 7,975, and 5,173 differentially methylated regions (DMRs) between control and stress groups were found in the F0, F1, and F2 generations, respectively. Inter- and transgenerational inheritance of paternal DMRs were at frequencies approximately 11.36% and 0.48%, respectively. These DMRs related to genes with functional implications for psychological stress response, and tissue inheritance of these DMRs passed paternal disorders epigenetically to offspring. More importantly, these DMRs evaded offspring embryonic reprogramming through erasure and subsequent reestablishment, but not via un-erasure way. Nonetheless, their reestablishment proportions in the primitive streak (E7.5) stage were altered. Furthermore, sncRNA-seq revealed that stress-induced tsRNA, miRNA and rsRNA dysregulation in paternal sperm might play important roles in DMRs occurrence and paternal inheritance.
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Project description:Parental environmental exposures can strongly influence descendant risks for adult disease. Metabolic disorders arise from the intersection of environmental and genetic risk factors, with epigenetic inheritance being at the center of the familial cycle of transgenerational disease. How paternal high-fat diet changes the sperm chromatin leading to the acquisition of metabolic disease in offspring remains controversial and ill-defined. Using a genetic model of epigenetic inheritance, we investigated the role of histone H3 lysine 4 methylation (H3K4me3) in the paternal transmission of metabolic dysfunction. We show that obesity-induced alterations in sperm H3K4me3 associated with offspring phenotypes and corresponded to embryonic and placental chromatin profiles and gene expression. Transgenerational susceptibility to metabolic disease was only observed when grandsires had a pre-existing genetic predisposition to metabolic dysfunction that was associated with enhanced alterations to sperm H3K4me3. This non-DNA based knowledge of inheritance has the potential to improve our understanding of how environment shapes heritability and may lead to novel routes for the prevention of disease.
2022-03-30 | GSE178096 | GEO
Project description:Ancestral environmental exposures that promote epigenetic transgenerational inheritance influence all aspects of an individual’s life history. Stress experienced during adolescence can affect adult physiological and behavioural phenotypes. The current study utilized a systems biology approach to investigate the interactions of these two forms of epigenetic modification, one carried in the germline transgenerationally and the other contained in the context of life history. A transgenerational epigenetic imprint left by the fungicide vinclozolin promoted regional specific brain gene networks that influenced chronic restraint stress responses to alter adult physiological, brain and behavioural phenotypes. The environmentally-induced epigenetic transgenerational inheritance was found to interact with early life stress response to impact the adult brain genome activity to bring “the phenotype into being”. We used microarrays to determine genes expressed differentially in rats' 4 brain areas - basolateral amygdala (BLA), primary and secondary motor cortex (Crtx), CA1 of the hippocampus (CA1), and CA3 of the hippocampus (CA3) - due to Vinclozolin treatments of their grand-grandmothers and/or to stress in adolescence age. For each of 4 brain areas (BLA, CRTX, CA1, and CA3), RNA samples from 4 treatment groups - stressed control (St-Con), non-stressed control (NSt-Con), stressed vinclozolin (St-Vin), and non-stressed vinclozolin (NSt-Vin) - were compared to each other. Each treatment groups contained 3 biological replica. RNA for each replica was pooled from 4 individual animals forming a certain dyad group.
2012-02-01 | E-GEOD-26737 | biostudies-arrayexpress
Project description:Epigenetic information can be inherited through the mammalian germline, and represents a plausible transgenerational carrier of environmental information. To test whether transgenerational inheritance of environmental information occurs in mammals, we carried out an expression profiling screen for genes in mice that responded to paternal diet. As part of this analysis, we chracterise the changes in sperm cytosine methylation in response to different diets. Characterizing the RNA exression changes in livers of offspring mice in response to the paternal diet, comparing between low-protein diet and control-diet. Examination the effect of 3 different paternal diets, control diet, Caloric Restriction and low-protein diet, on sperm cytosine methylation.
2011-01-14 | E-GEOD-25898 | biostudies-arrayexpress
Project description:Epigenetic signatures in germ cells, capable of both responding to the parental environment and shaping offspring neurodevelopment, are uniquely positioned to mediate transgenerational outcomes. However, molecular mechanisms by which these marks may communicate experience-dependent information across generations are currently unknown. In our model of chronic paternal stress, we previously identified nine microRNAs (miRs) that were increased in the sperm of stressed sires and associated with reduced hypothalamic-pituitary-adrenal (HPA) stress axis reactivity in offspring. In the current study, we rigorously examine the hypothesis that these sperm miRs function postfertilization to alter offspring stress responsivity and, using zygote microinjection of the nine specific miRs, demonstrated a remarkable recapitulation of the offspring stress dysregulation phenotype. Further, we associated long-term reprogramming of the hypothalamic transcriptome with HPA axis dysfunction, noting a marked decreased in the expression of extracellular matrix and collagen gene sets that may reflect an underlying change in blood-brain barrier permeability. We conclude by investigating the developmental impact of sperm miRs in early zygotes with single-cell amplification technology, identifying the targeted degradation of stored maternal mRNA transcripts including sirtuin 1 and ubiquitin protein ligase E3a, two genes with established function in chromatin remodeling, and this potent regulatory function of miRs postfertilization likely initiates a cascade of molecular events that eventually alters stress reactivity. Overall, these findings demonstrate a clear mechanistic role for sperm miRs in the transgenerational transmission of paternal lifetime experiences.
| S-EPMC4640733 | biostudies-literature
Project description:Genetic-epigenetic interactions in paternal transgenerational inheritance of metabolic disorders
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Project description:Epigenetic information can be inherited through the mammalian germline, and represents a plausible transgenerational carrier of environmental information. To test whether transgenerational inheritance of environmental information occurs in mammals, we carried out an expression profiling screen for genes in mice that responded to paternal diet. Characterizing the RNA exression changes in livers of offspring mice in response to the paternal diet, comparing between low-protein diet and control-diet. Examination of the effect of 2 different paternal diets, control diet and low-protein diet, on the mRNA expression in the liver of the offsprinngs. 26 samples: including Control diet vs. Low-protein (with dye swap), and Control diet vs. Low-protein after fasting the mice.
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Project description:Epigenetic information can be inherited through the mammalian germline, and represents a plausible transgenerational carrier of environmental information. To test whether transgenerational inheritance of environmental information occurs in mammals, we carried out an expression profiling screen for genes in mice that responded to paternal diet. Characterising the change in RNA expression in sperm in response to different paternal diets. Examination of the effect of different diets, control diet, low-protein diet and caloric-restriction diet, on the RNA expression in the sperm. 8 samples: 3 are control diets and 2 are low protein diets 1 caloric restriction diet, and 2 samples from Epidydimal tissue.
2011-01-14 | E-GEOD-25896 | biostudies-arrayexpress