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

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

PROVIDER: PRJEB82789 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR13994600_1.fastq.gz	Fastqsanger.gz
	ERR13994600_2.fastq.gz	Fastqsanger.gz
	ERR13994501_1.fastq.gz	Fastqsanger.gz
	ERR13994501_2.fastq.gz	Fastqsanger.gz
	ERR13994601_1.fastq.gz	Fastqsanger.gz

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

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

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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.

2024-11-22 | E-MTAB-14640 | biostudies-arrayexpress

Bulk transcriptomic profiles of mouse testes in response to male environmental exposures in the young FVB background

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2024-11-22 | E-MTAB-14637 | biostudies-arrayexpress

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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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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Project description:DNA demethylation of paternal genome in zygotes takes place in various mammals including mice and human. Recent studies have revealed that this is achieved through Tet3-mediated iterative oxidation of 5-methylcytosine (5mC) coupled with replication-dependent dilution. Tet3-mediated paternal DNA demethylation is believed to be required for mouse development given that Tet3 heterozygous embryos, derived by fertilizing Tet3 knockout (KO) oocytes with wild-type (WT) sperms, exhibit 5mC oxidation defects and embryonic sublethality, Here we demonstrate that the sublethality phenotype of the maternal KO mice is caused by haploinsufficiency of Tet3, but not by defective paternal 5mC oxidation. We found that Tet3 heterozygous mice derived from crosses of heterozygous father or mother with WT mice also exhibit sublethality phenotype similarly to Tet3 maternal KO mice. Importantly, embryos reconstituted with WT paternal nuclei that bypassed 5mC oxidation develop to term and grow to adulthood normally. Genome-scale DNA methylation analysis of the maternal KO zygotes and blastocysts demonstrated that hypermethylation caused by the depletion of maternal Tet3 is largely diminished by the blastocyst stage. Our study thus not only demonstrates that Tet3-mediated paternal 5mC oxidation is dispensable for mouse development but also suggests the existence of a compensation mechanism in preimplantation embryos that can compensate for the defective 5mC oxidation in zygotes. This data set includes RRBS data of wild-type and maternal Tet3 KO zygotes and blastocysts (C57BL/6J x CAST/EiJ)

2015-02-28 | E-GEOD-62719 | biostudies-arrayexpress

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Paternal microbiome perturbations impact offspring fitness

Project description:<p>The gut microbiota operates at the interface of host-environment interactions to influence human homeostasis and metabolic networks. Environmental factors that unbalance gut microbial ecosystems can therefore elicit physiological and disease-associated responses across somatic tissues. However, the systemic impact of the gut microbiome on the germline - and consequently on the F1 offspring it gives rise to - is unexplored. Here we show that the gut microbiota act as a key interface between paternal preconception environment and intergenerational health in mice. Perturbations to the gut microbiota of prospective fathers increase the probability of their offspring presenting with low birth weight, severe growth restriction and premature mortality. Transmission of disease risk occurs via the germline and is provoked by pervasive gut microbiome perturbations, including non-absorbable antibiotics or osmotic laxatives, but is rescued by restoring the paternal microbiota before conception. This effect is linked with a dynamic response to induced dysbiosis in the male reproductive system, including impaired leptin signalling, altered testicular metabolite profiles and remapped small RNA payloads in sperm. As a result, dysbiotic fathers trigger an elevated risk of in utero placental insufficiency, revealing a placental origin of mammalian intergenerational effects. Our study defines a regulatory ‘gut-germline axis’ in males, which is sensitive to environmental exposures and programs offspring fitness through impacting placental function.</p>

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