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Single-embryo transcriptomic profiles of mouse blastocysts in response to paternal environmental exposures in young C57BL/6J background

ABSTRACT: Single-embryo transcriptomic profiles of mouse blastocysts in response to paternal environmental exposures in young C57BL/6J background

PROVIDER: PRJEB82790 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR13994700_1.fastq.gz	Fastqsanger.gz
	ERR13994700_2.fastq.gz	Fastqsanger.gz
	ERR13994800_1.fastq.gz	Fastqsanger.gz
	ERR13994800_2.fastq.gz	Fastqsanger.gz
	ERR13994701_1.fastq.gz	Fastqsanger.gz

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Single-embryo transcriptomic profiles of mouse blastocysts in response to paternal environmental exposures in young FVB background

Project description:Single-embryo transcriptomic profiles of mouse blastocysts in response to paternal environmental exposures in young FVB background

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Single-embryo transcriptomic profiles of mouse blastocysts in response to paternal environmental exposures in young C57BL/6J background

Project description:This study includes raw data of blastocyst single-embryo SMART-seq profiles generated by IVF using sperm derived from treated (nABX & LPHS with nABX: non-absorbable antibiotics and LPHS: low-protein, high sugar diet) and control (CON) males of young (9-11 weeks) C57BL/6J background. After SMART-seq library preparation of single embryos, indexed samples were pooled and sequenced on the NextSeq 2000 using a P3 flow cell in 50bp paired-end mode, targeting an average of 5 million reads per sample.

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Single-embryo transcriptomic profiles of mouse blastocysts in response to paternal environmental exposures in young FVB background

Project description:This study includes raw data of blastocyst single-embryo SMART-seq profiles generated by IVF using sperm derived from treated (nABX & LPHS, with nABX: non-absorbable antibiotics and LPHS: low-protein, high sugar diet) and control (CON) males of young (9-10 weeks) FVB background. After SMART-seq library preparation of single embryos, indexed samples were pooled and sequenced on the NextSeq 2000 using a P3 flow cell in 50bp paired-end mode, targeting an average of 5 million reads per sample.

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Maternal DNMT3A-dependent de novo methylation of the zygotic paternal genome inhibits gene expression in the early embryo

Project description:De novo DNA methylation (DNAme) during mammalian spermatogenesis yields a densely methylated genome, with the exception of CpG islands (CGIs), which are hypomethylated in sperm. Following fertilization, the paternal genome undergoes widespread DNAme loss before the first S-phase. Paradoxically, recent mass spectrometry analysis revealed that a low level of de novo DNAme occurs exclusively on the zygotic paternal genome. However, the genomic loci involved and impact on genic transcription was not addressed. Here, we employ allele-specific analysis of whole-genome bisulphite sequencing (WGBS) data and show that a number of genomic loci, including several dozen CGI promoters, are de novo methylated on the paternal genome in 2-cell embryos. A subset of these promoters maintain DNAme through development to the blastocyst stage. Consistent with zygotic paternal DNAme acquisition (PDA), many of these loci are hypermethylated in androgenetic blastocysts but hypomethylated in parthenogenetic blastocysts. Strikingly, PDA is lost following maternal deletion of Dnmt3a. Furthermore, a subset of promoters showing PDA which are normally transcribed from the paternal allele in ICM cells show premature transcription at the 4C stage in maternal Dnmt3a knockout embryos. Taken together, these observations uncover an unexpected role for maternal DNMT3A activity in post-fertilization epigenetic reprogramming and transcriptional silencing of the paternal genome.

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Haploinsufficiency, but not defective paternal 5mC oxidation, accounts for the developmental defects of maternal Tet3 knockouts

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Single-embryo transcriptomic profiles of mouse blastocysts from mature and young males in the C57BL/6N background

Project description:Single-embryo transcriptomic profiles of mouse blastocysts from mature and young males in the C57BL/6N background

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Paternal exposure alone induces alcohol-related birth defects in a mouse model: Implications of paternal drinking in FAS birth defects.

Project description:Prevailing dogma maintains that Fetal Alcohol Syndrome (FAS) craniofacial and neurological birth defects are the sole consequence of maternal alcohol use during pregnancy. Using a physiologically relevant mouse model, we contrasted the incidence of alcohol-related growth and craniofacial defects between offspring derived from maternal, paternal, and dual parental alcohol exposures. Geometric morphometric analyses reveal that maternal, paternal, and dual parental exposures each induce unique craniofacial malformations and program dose-dependent increases in microcephaly, particularly in male offspring. Notably, dual parental exposures do not exhibit additive or synergistic effects; instead, our transcriptomic analyses demonstrate that each treatment programs distinct sex-specific changes in gene expression within the developing brain. Our data are the first to demonstrate that male drinking is a plausible driver of alcohol- related birth defects and that epidemiological examination of male alcohol consumption may help explain the enormous variation in FAS clinical presentations and severity.

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