Chromatin epimutations in transgenerational epigenetic inheritance
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA872365 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21176200_1.fastq.gz | Fastqsanger.gz | |||
| SRR21176200_2.fastq.gz | Fastqsanger.gz | |||
| SRR21176201_1.fastq.gz | Fastqsanger.gz | |||
| SRR21176201_2.fastq.gz | Fastqsanger.gz | |||
| SRR21176202_1.fastq.gz | Fastqsanger.gz |
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Project description:Epigenetic inheritance is the transmission of altered gene expression states across dividing cells without DNA sequence variation. Induced epigenetic changes (epimutations) have been extensively studied, but importantly, epimutations also occur spontaneously in a manner reminiscent of DNA sequence change. Small RNAs are established as a source of spontaneous epimutations which transmit gene expression changes over multiple generations in C.elegans. These changes are generally short lived, but rarely long-lived changes occur. Given that chromatin state is a critical regulator of gene expression, we explored whether chromatin states also undergo spontaneous change and whether this could be a potential alternative mechanism for transgenerational epigenetic inheritance. We compared the chromatin profiles and gene expression profiles at matched time points from a twenty generation bottlenecked lineage of C.elegans. We found that heritable changes in gene expression arose at a higher rate than the estimate for DNA sequence variation, indicating that these were true epigenetic events. In addition to recapitulating the known role for small RNAs, we provide evidence for chromatin mediated epimutations as an alternative mechanism driving epigenetic inheritance. Chromatin epimutations were heritable, enriched in the germline and synchronised with inherited gene expression changes. As with small RNA mediated epimutations, they were generally short lived with a tendency to resolve to baseline after 2-3 generations. A subset of chromatin epimutations however were long lasting, and these were uniquely enriched in piRNA clusters. Genes with long lived epimutations were implicated in multiple components of xenobiotic response pathways. This points to a mechanism for epigenetic ‘anticipation’ of environmental stressors. Adaptive traits driven by epimutations may be selected for under adverse conditions and lost on return to normal conditions, enabling soft adaptation in the absence of genetic sequence change.
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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:A variety of environmental factors have been shown to induce the epigenetic transgenerational inheritance of disease and phenotypic variation. This involves the germline transmission of epigenetic information between generations. Exposure specific sperm epimutations have been previously observed. The current study was designed to investigate the potential role genetic mutations have in the process, using copy number variations (CNV). In the first (F1) generation following exposure negligible CNV were identified, but in the transgenerational F3 generation a significant increase in CNV were identified in the sperm. The genome-wide differential DNA methylation regions (epimutations) were correlated with the genome locations of the CNV. Observations indicate the environmental induction of the epigenetic transgenerational inheritance of sperm epimutations promotes genome instability such that genetic CNV mutations are acquired in later generations. A combination of epigenetics and genetics is suggested to be involved in the transgenerational phenotypes.
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Project description:Environmental compounds have been shown to promote epigenetic transgenerational inheritance of disease. The current study was designed to determine if a hydrocarbon mixture involving jet fuel (JP-8) promotes epigenetic transgenerational inheritance of disease. Gestating F0 generation female rats were transiently exposed during the fetal gonadal development period. The direct exposure F1 generation had an increased incidence of kidney abnormalities in both females and males, prostate and pubertal abnormalities in males, and primordial follicle loss and polycystic ovarian disease in females. The first transgenerational generation is the F3 generation, and the jet fuel lineage had an increased incidence of primordial follicle loss and polycystic ovarian disease in females, and obesity in both females and males. Analysis of the jet fuel lineage F3 generation sperm epigenome identified 33 differential DNA methylation regions, termed epimutations. Observations demonstrate hydrocarbons can promote epigenetic transgenerational inheritance of disease and sperm epimutations, potential biomarkers for ancestral exposures. Methylated sperm DNA was isolated from rats ancestrally exposed to jet fuel (Jip). 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 (Jip1/Cip1, Jip2/Cip2, and Jip3/Cip3), resulting in three arrays for the treatment.
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Project description:A variety of environmental factors have been shown to induce the epigenetic transgenerational inheritance of disease and phenotypic variation. This involves the germline transmission of epigenetic information between generations. Exposure specific sperm epimutations have been previously observed. The current study was designed to investigate the potential role genetic mutations have in the process, using copy number variations (CNV). In the first (F1) generation following exposure negligible CNV were identified, but in the transgenerational F3 generation a significant increase in CNV were identified in the sperm. The genome-wide differential DNA methylation regions (epimutations) were correlated with the genome locations of the CNV. Observations indicate the environmental induction of the epigenetic transgenerational inheritance of sperm epimutations promotes genome instability such that genetic CNV mutations are acquired in later generations. A combination of epigenetics and genetics is suggested to be involved in the transgenerational phenotypes.
2015-04-01 | GSE62426 | GEO
Project description:Environmental compounds are known to promote epigenetic transgenerational inheritance of disease. The current study was designed to determine if a M-bM-^@M-^\pesticide mixtureM-bM-^@M-^] (pesticide permethrin and insect repellent N,N-Diethyl-meta-toluamide, DEET) promotes epigenetic transgenerational inheritance of disease and associated DNA methylation epimutations in sperm. Gestating F0 generation female rats were exposed during fetal gonadal sex determination and the incidence of disease evaluated in F1 and F3 generations. There were significant increases in the incidence of total diseases in animals from pesticide lineage F1 and F3 generation animals. Pubertal abnormalities, testis disease, and ovarian disease (primordial follicle loss and polycystic ovarian disease) were increased in F3 generation animals. Analysis of the pesticide lineage F3 generation sperm epigenome identified 363 differential DNA methylation regions (DMR) termed epimutations. Observations demonstrate that a pesticide mixture (permethrin and DEET) can promote epigenetic transgenerational inheritance of adult onset disease and potential sperm epigenetic biomarkers for ancestral environmental exposures. Methylated sperm DNA was isolated from rats ancestrally exposed to pesticides (Pip). 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 (Pip1/Cip1, Pip2/Cip2, and Pip3/Cip3), resulting in three arrays for the treatment.
2014-07-22 | E-GEOD-59554 | 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:Environmental compounds have been shown to promote epigenetic transgenerational inheritance of disease. The current study was designed to determine if a hydrocarbon mixture involving jet fuel (JP-8) promotes epigenetic transgenerational inheritance of disease. Gestating F0 generation female rats were transiently exposed during the fetal gonadal development period. The direct exposure F1 generation had an increased incidence of kidney abnormalities in both females and males, prostate and pubertal abnormalities in males, and primordial follicle loss and polycystic ovarian disease in females. The first transgenerational generation is the F3 generation, and the jet fuel lineage had an increased incidence of primordial follicle loss and polycystic ovarian disease in females, and obesity in both females and males. Analysis of the jet fuel lineage F3 generation sperm epigenome identified 33 differential DNA methylation regions, termed epimutations. Observations demonstrate hydrocarbons can promote epigenetic transgenerational inheritance of disease and sperm epimutations, potential biomarkers for ancestral exposures.
2014-07-22 | GSE59553 | GEO
Project description:Environmental compounds are known to promote epigenetic transgenerational inheritance of disease. The current study was designed to determine if a “pesticide mixture” (pesticide permethrin and insect repellent N,N-Diethyl-meta-toluamide, DEET) promotes epigenetic transgenerational inheritance of disease and associated DNA methylation epimutations in sperm. Gestating F0 generation female rats were exposed during fetal gonadal sex determination and the incidence of disease evaluated in F1 and F3 generations. There were significant increases in the incidence of total diseases in animals from pesticide lineage F1 and F3 generation animals. Pubertal abnormalities, testis disease, and ovarian disease (primordial follicle loss and polycystic ovarian disease) were increased in F3 generation animals. Analysis of the pesticide lineage F3 generation sperm epigenome identified 363 differential DNA methylation regions (DMR) termed epimutations. Observations demonstrate that a pesticide mixture (permethrin and DEET) can promote epigenetic transgenerational inheritance of adult onset disease and potential sperm epigenetic biomarkers for ancestral environmental exposures.
2014-07-22 | GSE59554 | GEO
Project description:Environmental compounds are known to promote epigenetic transgenerational inheritance of adult onset disease in subsequent generations (F1M-bM-^@M-^SF3) following ancestral exposure during fetal gonadal sex determination. The current study was designed to determine if a mixture of plastic derived endocrine disruptor compounds bisphenol-A (BPA), bis(2-ethylhexyl)phthalate (DEHP) and dibutyl phthalate (DBP) at two different doses promoted epigenetic transgenerational inheritance of adult onset disease and associated DNA methylation epimutations in sperm. Gestating F0 generation females were exposed to either the M-bM-^@M-^\plasticsM-bM-^@M-^] or M-bM-^@M-^\lower dose plasticsM-bM-^@M-^] mixture during embryonic days 8 to 14 of gonadal sex determination and the incidence of adult onset disease was evaluated in F1 and F3 generation rats. There were significant increases in the incidence of total disease/abnormalities in F1 and F3 generation male and female animals from plastics lineages. Pubertal abnormalities, testis disease, obesity, and ovarian disease (primary ovarian insufficiency and polycystic ovaries) were increased in the F3 generation animals. Kidney and prostate disease were only observed in the direct fetally exposed F1 generation plastic lineage animals. Analysis of the plastics lineage F3 generation sperm epigenome previously identified 197 differential DNA methylation regions (DMR) in gene promoters, termed epimutations. A number of these transgenerational DMR form a unique direct connection gene network and have previously been shown to correlate with the pathologies identified. Observations demonstrate that a mixture of plastic derived compounds, BPA and phthalates, can promote epigenetic transgenerational inheritance of adult onset disease. The sperm DMR provide potential epigenetic biomarkers for transgenerational disease and/or ancestral environmental exposures. Methylated sperm DNA was isolated from rats ancestrally exposed to plastics (Bip). 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 (Bip1/Cip1, Bip2/Cip2, and Bip3/Cip3), resulting in three arrays for the treatment.
2014-07-22 | E-GEOD-59555 | biostudies-arrayexpress