Epigenetic homogeneity underlies sperm programming for embryonic transcription
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA518148 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8515030_1.fastq.gz | Fastqsanger.gz | |||
| SRR8515030_2.fastq.gz | Fastqsanger.gz | |||
| SRR8515040.fastq.gz | Fastqsanger.gz | |||
| SRR8515050.fastq.gz | Fastqsanger.gz | |||
| SRR8515031_1.fastq.gz | Fastqsanger.gz |
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Project description:Epigenetic homogeneity underlies sperm programming for embryonic transcription single-ended ChIP-Seq libraries from sperm, egg extract (-geminin) treated sperm, egg extract (+geminin) treated sperm, and St 7 embryos with antibody for H3Kme3, H3K27me3, 3 replicates for each histone modification pull-down
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Project description:Sperm contributes genetic and epigenetic information to the embryo to efficiently support development. However, the mechanism underlying such developmental competence remains elusive. Here, we investigated whether all sperm cells have a common epigenetic configuration that primes transcriptional program for embryonic development. We show for the first time that remodelling of histones during spermiogenesis results in the retention of methylated histone H3 at the same genomic location in every sperm cell. This homogeneously methylated fraction of histone H3 in the sperm genome is maintained during early embryonic replication. Such methylated histone fraction resisting postfertilisation reprogramming marks developmental genes whose expression is perturbed upon experimental reduction of histone methylation. A similar homogeneously methylated histone H3 fraction is detected in human sperm. Altogether, we uncover a conserved mechanism of paternal epigenetic information transmission to the embryo through the homogeneous retention of methylated histone in a sperm cells population.
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Project description:Epigenetic programming of human sperm
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Project description:The WGBS data was published in PMID: 31393794 and the sequencing data from WGBS and MCC-Seq have been submitted to the European Genome-phenome Archive under the accession number EGAS00001003617. The paternal environment including stress, diet and toxicants has been linked to infertility and negative outcomes for offspring such as birth defects and adult onset of disease. Such effects may be transmitted via sperm through epigenetic mechanisms. To date, in depth profiling of the sperm epigenome in men has been limited. Our objective was to characterize the sperm profile of histone H3 lysine 4 tri-methylation (H3K4me3) from a reference population of men and relate this to sperm DNA methylation. ChIP-seq targeting H3K4me3 was performed on sperm from a representative reference population of 30 men and then overlapped with whole genome bisulfite sequencing (WGBS) data from the same men. Our analysis revealed that H3K4me3 is localized throughout the genome and at genes for fertility and development. Remarkably, enrichment was also found at regions that escape epigenetic reprogramming in primordial germ cells, embryonic enhancers and SINEs. The level of H3K4me3 in sperm associates with the degree of gene expression in embryo development. We find significant overlap in H3K4me3 and DNA methylation throughout the genome suggesting potential for the development of a personalized medicine approach for the assessment of fertility, lifestyle and environmental exposures.
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Project description:Preconception environmental conditions have been demonstrated to shape sperm epigenetics and subsequently offspring health and development. Our previous findings in humans showed that urinary anti-androgenic phthalate metabolites in males were associated with altered sperm methylation and blastocyst-stage embryo development. To corroborate this, we examined the effect of preconception exposure to di(2-ethylhexyl) phthalate (DEHP) on genome-wide DNA methylation and gene expression profiles in mice. We found that male preconception DEHP exposure resulted in 704 differentially methylated regions (DMRs; q-value < 0.05; ³ 10% methylation change) in sperm, 1,716 DMRs in embryonic, and 3,181 DMRs in extra-embryonic tissue. Of these, 29 DMRs overlapped between sperm and F1 tissues, half of which showed concordant methylation changes between F0 and F1 generations. F1 transcriptomes at E7.5 were also altered by male preconception DEHP exposure including developmental gene families such as Hox, Gata, and Sox. Additionally, gene ontology analyses of DMRs and differentially expressed genes showed enrichment of multiple developmental processes including embryonic development, pattern specification and morphogenesis.
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Project description:Obesity is a global rising problem with epidemiological dimension. Obese parents can have programming effects on their offspring leading to obesity and associated diseases in later life. This constitutes a vicious circle. Epidemiological data and studies in rodents demonstrated differential programming effects in male and female offspring, but the timing of their developmental origin is not known. This study investigated if sex-specific programming effects of parental obesity can already be detected in the pre-implantation period. Diet induced obese male or female mice were mated with normal-weight partners and blastocysts were recovered. Gene expression profiling revealed sex-specific responses of the blastocyst transcriptome to maternal and paternal obesity. The changes in the transcriptome of male blastocysts were more pronounced than those of female blastocysts, with a stronger impact of paternal than of maternal obesity. The sperm of obese mice revealed an increased abundance of several miRNAs compared to lean mice. Our study indicates that sex-specific programming effects of parental obesity already start in the pre‑implantation period and reveals specific alterations of the sperm miRNA profile as mechanistic link to programming effects of paternal obesity.
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Project description:The mammalian sperm genome is generally thought to be condensed and transcriptionally inert. Here we show that most promoters in mouse sperm contain elongating RNA polymerase II and are flanked by several positioned nucleosomes marked by a variety of active histone modifications. The sperm genome is bound by several transcription factors, including Nanog, Oct4, Mediator, condensin, and the pioneer factor FoxA1. These proteins are found at promoters, enhancers, and super-enhancers, many of which are active in mESCs or adult tissues. CTCF and cohesin are also present in sperm DNA, where they mediate interactions that organize the sperm genome into domains and compartments that overlap extensively with those found in mESCs. These results indicate that the sperm genome is rich in epigenetic information and primed for its expression during embryonic and adult life, and suggest mechanisms by which environmental effects on the paternal germline can be transmitted trans-generationally.
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Project description:The mammalian sperm genome is generally thought to be condensed and transcriptionally inert. Here we show that most promoters in mouse sperm contain elongating RNA polymerase II and are flanked by several positioned nucleosomes marked by a variety of active histone modifications. The sperm genome is bound by several transcription factors, including Nanog, Oct4, Mediator, condensin, and the pioneer factor FoxA1. These proteins are found at promoters, enhancers, and super-enhancers, many of which are active in mESCs or adult tissues. CTCF and cohesin are also present in sperm DNA, where they mediate interactions that organize the sperm genome into domains and compartments that overlap extensively with those found in mESCs. These results indicate that the sperm genome is rich in epigenetic information and primed for its expression during embryonic and adult life, and suggest mechanisms by which environmental effects on the paternal germline can be transmitted trans-generationally.
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