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Epigenetic reprogramming of sperm in F1 adult male mice with intrauterine hyperglycemia exposure

ABSTRACT: Epigenetic reprogramming of sperm in F1 adult male mice with intrauterine hyperglycemia exposure

PROVIDER: PRJNA597216 | ENA |

REPOSITORIES: ENA

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Epigenetic reprogramming of sperm in F1 adult male mice with intrauterine hyperglycemia exposure

Project description:Birth cohort studies and experimental investigations in animals link gestational diabetes mellitus (GDM) with impaired cognitive performance in the first filial generation (F1). We found that intrauterine hyperglycemia exposure resulted in behavior abnormality and cognitional functional disorder of both F1- and F2-GDM male mice. Methylome of sperm of F1 adult male mice from control pregnant mice (F1-C) and GDM pregnant mice (F1-GDM) revealed differentially methylated genes enriched in neurodevelopmental process.

2021-08-25 | GSE142502 | GEO

Intrauterine hyperglycemia exposure per se altered metabolic functions in F2 offspring via reprogramming F1 PGCs

Project description:Intrauterine hyperglycemia has been linked to an elevated risk of diabetes in next and further generations. Existing reports about transmission effects of intrauterine hyperglycemia have included both intrauterine and postnatal metabolic exposure factors, the impact of intrauterine hyperglycemia per se has not been separately assessed. To investigate effect of intrauterine hyperglycemia exposure per se on further generations, we selected non-phenotypic F1-GDM and F2-GDM male mice to examin metabolic changes in next generation and performed a methylome on day 13.5 primordial germ cells (PGCs) of F1-GDM male fetus to explore its underlying mechanism. We found that intrauterine hyperglycemia exposure per se resulted in obesity, insulin resistance and/or glucose intolerance in F2 male mice, and no changes in F3 male mice. Methylome of day 13.5 PGCs of F1-GDM male fetus revealed differently methylation genes enriched in obesity and diabetic pathogenesis. Methylation validation of targeted gene Fyn showed consistent hypo-methylation status in F1 PGCs, F1 fetal testis, sperm of F1/N-GDM mice, and somatic cells of F2-GDM male mice. While fetal testis of F2-GDM mice showed no alteration in Fyn methylation. Our data indicates that intrauterine hyperglycemia exposure per se contributes to metabolic changes in F2 but not F3 generation, by altering methylation erasure in PGCs of F1 generation.

2017-12-20 | GSE108319 | GEO

Gene expression in the F1 and F2 mouse hippocampus with intrauterine hyperglycemia exposure

Project description:Studies on human and animals suggest associations between gestational diabetes mellitus (GDM) with impaired cognitive performance in offspring. Using a mouse model of diabetes during pregnancy, we found that intrauterine hyperglycemia exposure resulted in memory impairment in both the first filial (F1) males and the second filial (F2) males from the F1 male offspring. The effects of intrauterine hyperglycemia exposure on F1 and F2 hippocampus gene expression were also examined.

2021-08-25 | GSE147039 | GEO

Gene expression in the F1 and F2 mouse hippocampus with intrauterine hyperglycemia exposure

Project description:Gene expression in the F1 and F2 mouse hippocampus with intrauterine hyperglycemia exposure

| PRJNA612832 | ENA

Intrauterine hyperglycemia exposure per se altered metabolic functions in F2 offspring via reprogramming F1 PGCs

Project description:Intrauterine hyperglycemia exposure per se altered metabolic functions in F2 offspring via reprogramming F1 PGCs

| PRJNA423101 | ENA

DNA methylation profiles of F1 mice sperm of the control group and arsenic group

Project description:Pregnant C3H mice were given tap water (control group) and tap water containing 85 ppm sodium arsenite from gestational day 8 to 18 (arsenic group), respectively. The DNA methylomes of sperm of F1 mice were investigated by RRBS method. The results showed that gestational arsenic exposure increased hypomethylated cytosines in the F1 sperm genome. The present study has indicated environmental impacts on sperm DNA methylome establishment.

2020-12-08 | GSE150500 | GEO

Intrauterine hyperglycemia exposure results in intergenerational inheritance via DNA methylation reprogramming on F1 PGCs.

Project description: Not available

| S-EPMC5968593 | biostudies-literature

RNA-seq transcriptome profiling of 1) C. elegans male germlines vs. oogenic germlines, and 2) male germlines, sperm, and F1 offspring germlines when offspring inherited sperm chromatin lacking H3K27me3.

Project description:Paternal contributions to epigenetic inheritance are not well understood. We report that in C. elegans sperm, the genome is packaged in nucleosomes and carries a histone-based epigenetic memory of gene expressions during spermatogenesis. In mature sperm, genes with spermatogenesis-specific expression are marked with both active and represseive histone modifications and genes with oogenesis-enriched expression are marked with active histone modifications. We showed that genes with oogenesis-enriched expression are in fact transcribed in spermatogenic germlines. We tested if sperm chromatin marking is necessary for germ cell development in offspring that inherit both sperm and oocyte chromosomes, using male parents that either can or cannot generate H3K27me3. Males homozygous for a mutation in mes-3, which encodes a member of the worm PRC2 complex, were mated with feminized mes-3/+ heterozygous worms to produce offspring that inherited sperm chromosomes lacking H3K27me3. We call these offspring M+P- or MpPm (Maternal chromosomes are + or plus for H3K27me3, Paternal chromosomes are - or minus for H3K27me3). Most of the resulting mes-3 homozygous M+P- offspring developed into sterile adults in this sensitized genetic background. In contrast, genetically identical control offspring that received appropriate H3K27me3-marked sperm chromosomes (M+P+ or MpPp) displayed low sterility. We compared genes mis-regulated in mes-3 male germlines versus control him-8 male germlines, mature sperm from those germlines, and germlines of mes-3 mutant F1 offspring that inherited sperm chromatin lacking H3K27me3 (M+P-) versus inherited sperm chromatin with H3K27me3 (M+P+), based on RNA-seq.

2018-07-23 | GSE115708 | GEO

Paternal DCHP exposure on F1 male liver transcriptome

Project description:Purpose: To investigate the effects of DCHP expoure on F1 male hepatic metabolic disorders Methods: 8 week male WT mice were exposed to DCHP by oral gavage for 4 weeks, 3 week old F1 male mice were fed with HFD for 9 weeks, glucose and insulin tolerant tests were performed at 10-11 week old, liver RNA was isolated for further transcriptome analysis Results: Mice from DCHP exposure sires displayed glucose/insulin resistant phenotype, together with upregulation in inflammatoy related genes in the liver

2023-05-24 | GSE215806 | GEO

BPA Gestational Exposure Affects F1 Capacitated Spermatozoa

Project description:Proteomic investigations of spermatozoa provide practical tools for distinguishing normal, functional spermatozoa from abnormal spermatozoa. Indeed, two-dimensional gel electrophoresis (2-DE) coupled with mass spectrometry (MS) applies high-throughput industrial applications to identify sperm-specific proteins indicative of chemical exposure. As such, a direct comparison of protein expression profiles between control and exposed cells returned a set of protein markers. Because mature mammalian spermatozoa are virtually incapable of protein synthesis, the predicted protein biomarkers in spermatozoa offer considerable stability for use in clinical application. In the current study, we applied 2-DE coupled with ESI-MS/MS to investigate the modified protein profile in F1 capacitated spermatozoa due to gestational bisphenol-A (BPA) exposure to ascertain whether these proteomic modifications could explain the observed functional alterations in spermatozoa.

2018-01-02 | PXD006829 | Pride

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