Genome-wide maps of DNA methylome during oocyte aging and its transgenerational inheritance
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PROVIDER: PRJNA689127 | ENA |
REPOSITORIES: ENA
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Project description:The goals of this study are to compare genome-wide DNA methylation levels in young and aged oocytes,and to investigate the transgenerational inheritance of methylome profiles in oocytes during natural aging. We apply a novel protocol of rapamycin to overcome the DNA methylation drift associated with oocyte aging. 8-week-old female mice were injected intraperitoneally with rapamycin or vehicle for 40 weeks. At the end of the experiment, females (48 weeks, F0) were paired with young adult (~4 mo old) males to produce F1 offspring (OF1 and ORaF1). An F2 generation (OF2 and ORaF2) resulted from mating F1 female at 44~48 weeks of age with young adult males. To generate YF1 and YF2 as normal control (offspring of young mother), we mated females (~8 weeks) with young adult males. Then we collect oocytes (F0,F1 and F2 generations)，sperm ( F1 and F2 generations) and hippocampus (F1 female offspring) from different groups to investigate the transgenerational inheritance of DNA methylome profiles associated with oocyte aging by the single cell whole-genome methylation sequencing (sc-WGBS). We found that oocytes from aged mother exhibited increased DNA methylation levels in CpG sites. Maternal aging related methylome changes can be inherited transgenerationally though oocyte to the germ line of F1 and F2 offspring. The application of rapamycin during the course of oocyte aging could reverse these DNA methylation alterations, and it can ameliorate several neurobehavioral aging trails that were in observed in aged oocyte offspring. WGBS-seq on DNA from hippocampal tissue revealed a number of differentially methylated (P<0.05) genes in OF1 and ORaF1 compared with YF1, and some of the enriched pathways were associated with aging process, such as PI3K-Akt signaling pathway (akin to transcriptional alterations above), MAPK signaling and Ras signaling pathway .
2022-12-31 | GSE164139 | GEO
Project description:Some epigenetic modifications are inherited from one generation to the next, providing a potential mechanism for the inheritance of environmentally acquired traits. Transgenerational inheritance of RNA interference phenotypes in C. elegans provides an excellent model to study this phenomenon, and whilst studies have implicated both chromatin modifications and small RNA pathways in heritable silencing their relative contributions remain unclear. Here we demonstrate that the histone methyltransferases SET-25 and SET-32 are required for the establishment of a transgenerational silencing signal, but not for long-term maintenance of this signal between subsequent generations suggesting that transgenerational epigenetic inheritance is a multi-step process, with distinct genetic requirements for establishment and maintenance of heritable silencing. Furthermore, small RNA sequencing reveals that the abundance of secondary siRNA (thought to be the effector molecules of heritable silencing) does not correlate with silencing phenotypes. Together, our results suggest that the current mechanistic models of epigenetic inheritance are incomplete.
2018-10-30 | PXD008754 | Pride
Project description:5-methylcytosine is a major epigenetic modification sometimes called "the fifth nucleotide". However, our knowledge of how offspring inherit the DNA methylome from parents is limited. We generated nine single-base resolution DNA methylomes including zebrafish gametes and early embryos. The oocyte methylome is significantly hypo-methylated compared to sperm. Strikingly, the paternal DNA methylation pattern is maintained throughout early embryogenesis. The maternal DNA methylation pattern is maintained until the 16-cell stage. Then, the oocyte methylome is gradually discarded through cell division, and progressively reprogrammed to a pattern similar to that of the sperm methylome. The passive demethylation rate and the de novo methylation rate are similar in the maternal DNA. By the midblastula stage, the embryo?s methylome is virtually identical to the sperm methylome. Moreover, inheritance of the sperm methylome facilitates the epigenetic regulation of embryogenesis. Therefore, besides DNA sequences, sperm DNA methylome is also inherited in zebrafish early embryos.
2013-05-20 | GSE44075 | GEO
Project description:Transcriptome analysis in transgenerational epigenetic inheritance
| PRJNA922492 | ENA
Project description:Stress Resets Transgenerational Small RNA Inheritance
| PRJNA533340 | ENA
Project description:Chromatin epimutations in transgenerational epigenetic inheritance
| PRJNA872365 | ENA
Project description:5-methylcytosine is a major epigenetic modification sometimes called "the fifth nucleotide". However, our knowledge of how offspring inherit the DNA methylome from parents is limited. We generated nine single-base resolution DNA methylomes including zebrafish gametes and early embryos. The oocyte methylome is significantly hypo-methylated compared to sperm. Strikingly, the paternal DNA methylation pattern is maintained throughout early embryogenesis. The maternal DNA methylation pattern is maintained until the 16-cell stage. Then, the oocyte methylome is gradually discarded through cell division, and progressively reprogrammed to a pattern similar to that of the sperm methylome. The passive demethylation rate and the de novo methylation rate are similar in the maternal DNA. By the midblastula stage, the embryo?s methylome is virtually identical to the sperm methylome. Moreover, inheritance of the sperm methylome facilitates the epigenetic regulation of embryogenesis. Therefore, besides DNA sequences, sperm DNA methylome is also inherited in zebrafish early embryos. hMeDIP-seq is performed in sperm,2-cell,16-cell,1k-cell and a input control sample 4 new samples are added to GSE44075. RNA-seq is performed in sperm, egg,1k-cell, germring samples .hMeDIP-seq is performed in sperm,2-cell,16-cell,1k-cell and a input control sample 10 new samples are added to GSE44075. Bisulfite-seq is performed for nine samples : sperm, egg,16-cell,32-cell,64-cell,128-cell,1k-cell , Germring and testis. TAB-seq is performed for one sample , 32-cell.
2013-05-20 | E-GEOD-44075 | biostudies-arrayexpress
Project description:Environmentally induced epigenetic transgenerational inheritance of adult onset disease involves a variety of phenotypic changes suggesting a general alteration in genome activity. Investigation of eleven different tissue transcriptomes in male and female F3 generation vinclozolin versus control lineage rats demonstrated all tissues examined had unique transgenerational transcriptomes. Common cellular pathways and processes were identified among the tissues. A bionetwork analysis identified gene modules with coordinated gene expression and each had unique gene networks regulating tissue specific gene expression and function. A large number of statistically significant over-represented clusters of differentially expressed genes were identified and termed M-bM-^@M-^\Epigenetic Control RegionsM-bM-^@M-^]. Combined observations demonstrate that all tissues derived from the epigenetically altered germ line develop transgenerational transcriptomes unique to the tissue, but common epigenetic control regions in the genome appear to in part coordinately regulate these tissue specific transcriptomes. This systems biology approach provides insight into the molecular mechanisms involved in the epigenetic transgenerational inheritance of a variety of adult onset disease phenotypes. We used microarrays to determine genes expressed differentially in rats 11 male or female smatic tissues -male heart, kidney, liver, testis, prostate, seminal vesicles; female heart, kidney, liver, ovary, uterus - due to Vinclozolin treatments of their grand-grandmothers. For each of 11 male or female smatic tissues, RNA samples from 2 treatment groups - control (Con) and vinclozolin (Vin) - were compared to each other. Each treatment groups contained 3 biological replica. RNA for each replica was pooled from 2 individual animals.
2012-06-30 | E-GEOD-35839 | biostudies-arrayexpress
Project description:Transgenerational inheritance is challenging basic concepts of heredity and achieving control over such responses is of great interest. In C. elegans nematodes, small RNAs are transmitted across generations to establish a transgenerational memory trace of ancestral environments. Inheritance of small RNAs is regulated by dedicated machinery and can be tuned by outside cues. Carryover of aberrant heritable small RNA responses was shown to be maladaptive and to induce sterility in certain cases. Here we show that various types of stress (starvation, high temperatures, and hyperosmotic conditions) but not non-stressful changes in cultivation, lead to resetting of small RNA inheritance. We found that stress leads to a genome-wide reduction in heritable small RNA levels and that mutants defective in different stress pathways exhibit irregular RNAi inheritance dynamics. Moreover, we discovered that resetting of heritable RNAi is orchestrated by MAPK pathway factors, the transcription factor SKN-1, and the MET-2 methyltransferase. Termination of small RNA inheritance, and the fact that this process depends on stress, could protect from run-on of environment-irrelevant heritable gene regulation.
2021-03-24 | GSE129988 | GEO
Project description:Transgenerational inheritance of acquired traits/characteristics from ancestors is believed to play important roles in evolution, as well as health problems/symptoms not due to “classical genetic inheritance”. However, the central enigma, such as how the acquired transgenerational characteristics are developed, and how the acquired traits are transmitted from generations to generations of offspring, largely remained veiled. In this study, we used C elegans as a model system and provide evidence that the dynamic of H3K27me3 as a hallmark and regulator for the gut-mediated transgenerational inheritance of acquired traits. Further, we demonstrate that yolk proteins guide the establishment of the acquired epigenetic imprints in soma, as well as determines the transgenerational inheritance of epigenetic imprints and subsequent acquired behavior in offspring by maternal provision. Taken together, our findings support that yolk proteins both function as a systemic “non-nuclear factor” for establishing the somatic epigenetic imprints and as a “cargo” to transmit acquired epigenetic information to the subsequent generations through oocytes.
2022-09-10 | GSE138059 | GEO