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Small RNA reads sperm parental obesity

ABSTRACT: Sex-specific programming effects of parental obesity in pre-implantation embryonic development_small RNASeq Data of Sperm

PROVIDER: PRJEB33337 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	ERR3414560.fastq.gz	Fastqsanger.gz
	ERR3414561.fastq.gz	Fastqsanger.gz
	ERR3414562.fastq.gz	Fastqsanger.gz
	ERR3414563.fastq.gz	Fastqsanger.gz

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Sex-specific programming effects of parental obesity in pre-implantation embryonic development [RNASeq Data of Sperm]

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.

2019-07-07 | GSE133915 | GEO

Sex-specific programming effects of parental obesity in pre-implantation embryonic development [RNASeq Data of Oocytes]

2019-07-07 | GSE133914 | GEO

Sex-specific programming effects of parental obesity in pre-implantation embryonic development_Microarray data on blastocyst transcriptomes

2019-07-04 | GSE133767 | GEO

Sex-specific programming effects of parental obesity in pre-implantation embryonic development [RNASeq Data of Sperm]

Project description:Sex-specific programming effects of parental obesity in pre-implantation embryonic development [RNASeq Data of Sperm]

| PRJNA553001 | ENA

Sex-specific programming effects of parental obesity in pre-implantation embryonic development

Project description:Sex-specific programming effects of parental obesity in pre-implantation embryonic development

| PRJNA553000 | ENA

Sex-specific programming effects of parental obesity in pre-implantation embryonic development [RNASeq Data of Oocytes]

Project description:Sex-specific programming effects of parental obesity in pre-implantation embryonic development [RNASeq Data of Oocytes]

| PRJNA553002 | ENA

Sex-specific programming effects of parental obesity in pre-implantation embryonic development_Microarray data on blastocyst transcriptomes

Project description:Sex-specific programming effects of parental obesity in pre-implantation embryonic development_Microarray data on blastocyst transcriptomes

| PRJNA552488 | ENA

Paternal obesity alters the sperm epigenome and and is associated with changes in the placental transcriptome and its cellular composition [RNA-seq]

Project description:Growing evidence point towards a strong contribution of paternal factors in placental health with implications in adult-onset complex disease risk. We have recently demonstrated that paternal diet-induced obesity alters sperm histone methylation and is associated with metabolic disturbances in the next generation. Diet-sensitive epigenetic regions in sperm were found at genes involved in trophectoderm and placental development, and corresponded to epigenetic and gene expression profiles in these tissues. We sought to investigate whether paternal diet-induced obesity before conception can alter the placental transcriptome, and whether differential gene expression corresponds with sperm obesity-associated epigenetic signatures. C57BL6/J males were fed either a control or high-fat diet for 10 weeks beginning at 6 weeks of age. They were then bred to control-fed C57BL6/J females to induce pregnancies and E14.5 placentas were collected. RNA-sequencing was performed (n=4 per group per sex) to detect sex-specific transcriptional changes associated with paternal diet. At necropsy, sperm was collected for chromatin immunoprecipitation followed by sequencing (ChIP-seq; n=3 per group) targeting histone H3 lysine 4 tri-methylation (H3K4me3) to detect obesity-induced changes in H3K4me3 enrichment. There were sex-specific differentially expressed genes in placentas with some overlapping with promoters showing obesity-associated sperm epimutations. A deconvolution analysis using single-cell RNA-seq data from mouse E14.5 placenta (Han et al., Cell, 2018) revealed significant differences in trophoblast subtype proportions in placentas derived from HFD sires. This study highlights a previously underappreciated role of the placenta at the origin of paternally-induced metabolic disturbances in offspring.

2022-09-09 | GSE207313 | GEO

Paternal obesity alters the sperm epigenome and and is associated with changes in the placental transcriptome and its cellular composition [ChIP-seq]

2022-09-09 | GSE207325 | GEO

Paternal obesity-induced changes in sperm chromatin accessibility and have mild effect on offspring metabolic health

Project description:The increasing global burden of metabolic disorders including obesity and diabetes necessitates a comprehensive understanding of their etiology, which not only encompasses genetic and environmental factors but also parental influence. Recent evidence has unveiled paternal obesity as a contributing factor to offspring's metabolic health via sperm epigenetic modifications. In this study, we investigated the impact of a Western diet-induced obesity in C57BL/6 male mice on sperm chromatin accessibility and the subsequent metabolic health of their progeny. Utilizing Assay for Transposase-Accessible Chromatin with sequencing, we discovered 450 regions with differential accessibility in sperm from obese fathers, implicating key developmental and metabolic pathways. Contrary to expectations, these epigenetic alterations in sperm were not predictive of long-term metabolic disorders in offspring, who exhibited only mild transient metabolic changes early in life. Both male and female F1 progeny showed no enduring predisposition to obesity or diabetes. These results underscore the biological resilience of offspring to paternal epigenetic inheritance, suggesting a complex interplay between inherited epigenetic modifications and the offspring's own developmental compensatory mechanisms. This study calls for further research into the biological processes that confer this resilience, which could inform interventional strategies to combat the heritability of metabolic diseases.

2024-07-10 | GSE263011 | GEO

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