Maternal gestational nutrition perturbs offspring sperm epigenome in sheep
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ABSTRACT:
PROVIDER: PRJNA938147 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23598470_1.fastq.gz | Fastqsanger.gz | |||
| SRR23598470_2.fastq.gz | Fastqsanger.gz | |||
| SRR23598471_1.fastq.gz | Fastqsanger.gz | |||
| SRR23598471_2.fastq.gz | Fastqsanger.gz | |||
| SRR23598472_1.fastq.gz | Fastqsanger.gz |
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Project description:There is a growing body of evidence that inadequate maternal nutrition during gestation can have immediate and life-long effects on offspring. However, little is known about the reproductive effects of maternal gestational nutrition in offspring males. Here, using a sheep model of poor maternal nutrition (restricted- or over-feeding) during gestation, we found that poor maternal gestational nutrition does not affect semen characteristics (i.e. volume, sperm concentration, pH, sperm motility, sperm morphology) and scrotal circumference in offspring. However, by evaluating associations between poor maternal gestational nutrition and altered small non-cording RNAs (sncRNAs) and DNA methylation in offspring sperm, we demonstrated that poor maternal gestational nutrition alters sperm sncRNA composition and expression. Whole genome bisulfite sequencing further identified genomic regions with increased or decreased DNA methylation in sperm in response to poor maternal gestational nutrition. These findings imply that maternal diet-induced epigenetic errors can accumulate in sperm to worsen developmental outcomes of future generations.
2024-04-04 | GSE225924 | GEO
Project description:There is a growing body of evidence that inadequate maternal nutrition during gestation can have immediate and life-long effects on offspring. However, little is known about the reproductive effects of maternal gestational nutrition in offspring males. Here, using a sheep model of poor maternal nutrition (restricted- or over-feeding) during gestation, we found that poor maternal gestational nutrition does not affect semen characteristics (i.e. volume, sperm concentration, pH, sperm motility, sperm morphology) and scrotal circumference in offspring. However, by evaluating associations between poor maternal gestational nutrition and altered small non-cording RNAs (sncRNAs) and DNA methylation in offspring sperm, we demonstrated that poor maternal gestational nutrition alters sperm sncRNA composition and expression. Whole genome bisulfite sequencing further identified genomic regions with increased or decreased DNA methylation in sperm in response to poor maternal gestational nutrition. These findings imply that maternal diet-induced epigenetic errors can accumulate in sperm to worsen developmental outcomes of future generations.
2024-04-04 | GSE225985 | GEO
Project description:Maternal gestational nutrition perturbs offspring sperm epigenome in sheep [BiSulfite-seq]
| PRJNA938069 | ENA
Project description:Maternal gestational nutrition perturbs offspring sperm epigenome in sheep [ncRNA-seq]
| PRJNA938145 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-04-04 | GSE225988 | GEO
Project description:Compelling evidence supports that gestational chronodisruption induces major changes in maternal circadian rhythms, fetal development and that these changes impact adult life at many physiological levels. Using a rat model of chronic photoperiod shifting throughout gestation (CPS), we investigated the detrimental effects of gestational CPS on glucose homeostasis, adipose tissue physiology and metabolism in the adult male offspring. At proteomic level, in CPS adipose tissue, 275 proteins displayed differential expression, compared with LD animals fed with a standard diet. Interestingly, CPS offspring and LD fed with HFD showed 20 proteins in common (2 upregulated 18 downregulated). Based on these common proteins, the IPA analysis found that 2 functional pathways were significantly altered; the network 1 (AKT/ERK) and the network 2 (TNF/IL4).
2021-08-11 | PXD026315 | Pride
Project description:We hypothesized that poor maternal nutrition during gestation would reduce the growth and development of offspring muscle prenatally, reduce the number of myogenic progenitor cells, and result in changes in the global expression of genes involved in prenatal muscle development and function. Ewes were fed a control (100% NRC)-, restricted (60% NRC),- or over-fed (140% NRC) diet beginning at day 30 of gestation until day 45, 90, and 135 of gestation or until parturition. In offspring, we report altered secondary: primary muscle fiber ratios and percent PAX7 positive cells during fetal development. In addition, changes in muscle mRNA expression were observed between maternal dietary treatments and over timepoints during gestation. In conclusion, poor maternal nutrition during gestation contributes to altered offspring muscle growth during early fetal development which persists throughout the fetal stage.
2019-12-01 | GSE124327 | GEO
Project description:We evaluated if a higher plane of maternal nutrition during late gestation and weaning age alters the offspringM-bM-^@M-^Ys Longissimus muscle (LM) transcriptome. A microarray analysis was performed in LM samples of early (EW) and normal weaned (NW) Angus M-CM-^W Simmental calves born from cows that were grazing endophyte-infected tall fescue/red clover pastures with no supplement (low plane of nutrition (LPN)), or supplemented with 2.3 kg of dried distillerM-bM-^@M-^Ys grains with solubles and soyhulls (70% DDGS/30% soyhulls) (medium plane of nutrition (MPN)) during the last 90 days of gestation. Biopsies were harvested at 78, 187 and 354 days of age. Bioinformatics analysis highlighted that offspring transcriptome did not respond markedly to cow plane of nutrition, resulting in only 13 differentially expressed genes. However, weaning age and a high-starch diet strongly impacted the transcriptome, especially the immediate activation of the lipogenic program in EW steers. In addition, between 78 and 187 days of age, these animals had an activation of the innate immune system due presumably to macrophage infiltration in intramuscular fat. Between 187 and 354 days of age (i.e. the fattening phase), NW steers had an activation of the lipogenic transcriptome machinery, while EW steers had a clear gene transcription inhibition. The latter appears to have occurred through the epigenetic control of histone acetylases, which were down-regulated. Higher cow plane of nutrition alone affected 35 genes in the LM of steers that underscore the presence of a mechanism of macrophage infiltration likely originating from localized oxidative stress as a result of increased levels of hypoplasia and hypertrophy in LM. A subset of 20 Angus x Simmental beef cows from the University of Illinois Dixon Springs Agriculture Center (DSAC) in Simpson, IL, were selected from a group of animals utilized in a parallel study75. Main effects evaluated were maternal plane of nutrition during late gestation and postnatal management of the offspring. Three months prior to the projected parturition date cows were assigned to treatments (low or medium plane of nutrition) in a split-plot design. Low plane of nutrition (LPN) was achieved by grazing endophyte-infected tall fescue/red clover pastures during July, August, and September with no supplement. Medium plane of nutrition cow diet (MPN) was achieved by grazing endophyte-infected tall fescue/red clover pastures supplemented with 2.3 kg of dried distillerM-bM-^@M-^Ys grains with solubles and soyhulls (70% DDGS/30% soyhulls). Angus x Simmental steer calves were randomly assigned to early or normal weaning treatments within each gestational treatment. This allowed for 10 animals for each postnatal treatment and 5 animals of each of the interactions of gestational M-CM-^W postnatal treatments. At 78 M-BM-1 2 days postpartum, early-wean offspring were weaned, transported to Urbana Beef Unit, and adapted to a high-starch diet until they had ad libitum consumption. At 187 M-BM-1 2 days postpartum, normal-wean offspring were weaned and transported to Urbana Beef Unit. All offspring were co-mingled among treatments. LM biopsies were sampled from a subset of 5 animals per gestational M-CM-^W postnatal treatment at time of early weaning (~78 days) and at time of normal weaning (~187 days), and during the last week prior to harvest (~ 354 days). After normal weaning, all offspring were placed on a common, corn grain-based high-starch finishing diet that is typical of industry management (CP% = 18.1, NDF% = 25.3, ADF% = 14.3, crude fat % = 5.1). All the offspring in the study were harvested at a commercial packing plant when they reached the selected end point target back fat thickness of 1.1 cm. Reported final body weight (BW) was calculated from hot carcass weight using a 62% dressing percentage. In the present study, we used a transcriptome-wide bovine microarray (Agilent-015354 Bovine Oligo Microarray-4x44K) that contains 21,475 unique genes and transcripts of Bos Taurus, with two probes per gene. The methods used for hybridization and scanning were according to manufacturerM-bM-^@M-^Ys protocols and Loor et al45. The microarray data were deposited in the National Center for Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) database (http://www.ncbi.nlm.nih.gov/gds) with accession number GSE-XXXX. GeneSpring GX (Agilent Technologies) was used for data visualization and preliminary data mining. Subsequently, the entire microarray data set with associated statistical P-values were imported into Ingenuity Pathways Analysis M-BM-. (IPA, www.ingenuity.com) in order to examine the number of activated and inhibited differentially expressed genes (DEG). Entrez Gene IDs were used to identify individual sequences. Data from the microarray analysis were normalized for dye and microarray effects (i.e., Lowess normalization and array centering) and used for statistical analysis. The MIXED procedure of SAS (SAS Institute, Inc., Cary, NC, USA) was used for statistical analysis. Fixed effects were treatment (early weaning, normal weaning), diet (low and medium cow plane of nutrition), time (78, 187, and 354 days of age), first, second and third order interactions between diet, time and treatment, and dye (Cy3, Cy5) and random effects included steer and microarray. Raw P values were adjusted using Benjamini and HochbergM-bM-^@M-^Ys false discovery rate (FDR). Bioinformatics analysis of microarray data was performed using DIA 10 and information from the freely-available online databases Kyoto Encyclopedia of Genes and Genomes (KEGG) and Database for Annotation, Visualization, and Integrated Discovery (DAVID) v6.7 databases. A list of gene identifiers (Entrez Gene IDs) was uploaded all at once to extract and summarize functional annotations associated with groups of genes or with each individual gene. The significance value associated with biological processes and pathways is a measure of the likelihood that the distribution of DEG in these pathways and biological processes is due to chance. The significance is expressed as a P-value, which is calculated using the right-tailed Fisher's Exact Test and adjusted using FDR. Details of the DIA approach and its validation have been reported previously. The interpretation of the bioinformatics analysis was performed following the same approach as our previous study.
2015-02-03 | E-GEOD-65560 | biostudies-arrayexpress
Project description:Gestational diabetes is a common medical complication of pregnancy that is associated with adverse perinatal outcomes and an increased risk of metabolic diseases and atherosclerosis in adult offspring. The mechanisms responsible for this delayed pathological transmission remain unknown. In mouse models, we found that the development of atherosclerosis in adult offspring born to diabetic pregnancy can be in part linked to hematopoietic alterations. Although they do not show any gross metabolic disruptions, the adult offspring maintain hematopoietic features associated with diabetes, indicating the acquisition of a lasting diabetic hematopoietic memory. We show that the induction of this hematopoietic memory during gestation relies on the activity of the pattern recognition receptor AGER and the NLRP3 inflammasome, which leads to increased placental inflammation. In adult offspring, we find that this memory is associated with DNMT1 upregulation and epigenetic changes in hematopoietic progenitors. Altogether, our results demonstrate that the hematopoietic system can acquire a lasting memory of gestational diabetes, and that this memory constitutes a new pathway connecting gestational health to adult pathologies.
2023-11-13 | GSE244697 | GEO
Project description:Gestational diabetes is a common medical complication of pregnancy that is associated with adverse perinatal outcomes and an increased risk of metabolic diseases and atherosclerosis in adult offspring. The mechanisms responsible for this delayed pathological transmission remain unknown. In mouse models, we found that the development of atherosclerosis in adult offspring born to diabetic pregnancy can be in part linked to hematopoietic alterations. Although they do not show any gross metabolic disruptions, the adult offspring maintain hematopoietic features associated with diabetes, indicating the acquisition of a lasting diabetic hematopoietic memory. We show that the induction of this hematopoietic memory during gestation relies on the activity of the pattern recognition receptor AGER and the NLRP3 inflammasome, which leads to increased placental inflammation. In adult offspring, we find that this memory is associated with DNMT1 upregulation and epigenetic changes in hematopoietic progenitors. Altogether, our results demonstrate that the hematopoietic system can acquire a lasting memory of gestational diabetes, and that this memory constitutes a new pathway connecting gestational health to adult pathologies.
2023-11-13 | GSE244695 | GEO