Transgenerational inheritance of epigenetic signatures at CpG islands in mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA674639 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12982373_1.fastq.gz | Fastqsanger.gz | |||
| SRR12982373_2.fastq.gz | Fastqsanger.gz | |||
| SRR12982374_1.fastq.gz | Fastqsanger.gz | |||
| SRR12982374_2.fastq.gz | Fastqsanger.gz | |||
| SRR12982375_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 44 |
Similar Datasets
Project description:Transgenerational epigenetic inheritance in mammals remains a subject of debate. Here we demonstrate that DNA methylation of promoter-associated CpG islands (CGIs) can be transmitted from parents to their offspring in mice. We generated DNA methylation-edited mouse embryonic stem cells (ESCs) in which CGIs of two metabolism related genes, the Ankyrin repeat domain 26 and the low-density lipoprotein receptor, were specifically methylated and silenced. DNA methylation-edited mice generated by microinjection of the methylated ESCs exhibited abnormal metabolic phenotypes. Both the acquired methylation of the targeted CGI and the phenotypic traits were maintained and transmitted across multiple generations. The heritable CGI methylation was subjected to reprograming in parental PGCs and subsequently reestablished in the next generation at post-implantation stages. These observations provide a first concrete step in support of transgenerational epigenetic inheritance in mammals, which may allow for a better understanding of the etiology, diagnosis and prevention of non-genetically inherited human diseases.
2023-02-07 | GSE160847 | GEO
Project description:Previous studies have suggested an erasure of DNA methylation is required to develop the stem cells in the morula embryo. An exception involves imprinted genes that escape this DNA methylation erasure. Transgenerational differential DNA methylation regions (DMRs) have been speculated to also escape this erasure. The current study was designed to assess if morula embryos escape erasure of DDT (dichloro-diphenyl-trichloroethane)-induced transgenerational sperm DMRs. Observations demonstrate that the transgenerational sperm DMR sites are not erased, so are imprinted-like DMR sites. Interestingly, we also found that the majority of low-density CpG genomic sites had a significant increase in DNA methylation in the morula embryo compared to sperm. The general erasure of DNA methylation during embryogenesis appears applicable for high-density CpG islands, but not low-density CpG deserts.
2022-11-10 | GSE211135 | 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:CpG islands shape the epigenome landscape.
| PRJNA419733 | ENA
Project description:CpG island elements are associated with most mammalian gene promoters, yet how they contribute to gene regulation remains poorly understood. Recently it has become clear that a subset of CpG islands in embryonic stem cells can act as polycomb response elements and are recognized by the polycomb silencing systems to regulate the expression of genes involved in pluripotency and early developmental transcription programs. How CpG islands function mechanistically as nucleation sites for polycomb repressive complexes remains unknown. Here we discover that the KDM2B protein, by virtue of its ZF-CxxC DNA binding domain, specifically recognizes non-methylated DNA in CpG islands elements genome-wide. Through a physical interaction with the polycomb repressive complex 1 (PRC1), KDM2B targets PRC1 to CpG islands where it contributes to H2AK119ub1 and gene repression at a subset of polycomb targets. Unexpectedly, we also find that CpG islands are occupied by low levels of PRC1 throughout the genome, suggesting that the KDM2B-PRC1 complex may sample CpG island associated genes for susceptibility to polycomb mediated silencing. These observations demonstrate an unexpected and direct link between recognition of CpG islands by KDM2B and targeting of the polycomb repressive system. This provides the basis for a new model describing the functionality of CpG islands as mammalian PREs.
2012-12-26 | GSE40860 | GEO
Project description:Chromatin epimutations in transgenerational epigenetic inheritance
| PRJNA872365 | ENA
Project description:Transcriptome analysis in transgenerational epigenetic inheritance
| PRJNA922492 | ENA
Project description:Stress Resets Transgenerational Small RNA Inheritance
| PRJNA533340 | ENA
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