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Low paternal dietary folate alters the sperm epigenome and is associated with negative pregnancy outcomes

ABSTRACT: Epidemiological studies suggest that a fatherâ€™s diet can influence offspring health. A proposed mechanism for paternal transmission of environmental information is via the sperm epigenome. The epigenome includes heritable information such as DNA methylation. We hypothesized that the dietary supply of methyl donors would alter epigenetic reprogramming in sperm. This hypothesis was examined by feeding male mice a folate deficient (FD) and folate sufficient (FS) diets and then generating and analyzing DNA methylation profiles of their sperm.

ORGANISM(S): Mus musculus

PROVIDER: GSE52017 | GEO | 2013/11/02

SECONDARY ACCESSION(S): PRJNA226108

REPOSITORIES: GEO

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Low paternal dietary folate alters the sperm epigenome and is associated with negative pregnancy outcomes

Project description:Epidemiological studies suggest that a fatherâ€™s diet can influence offspring health. A proposed mechanism for paternal transmission of environmental information is via the sperm epigenome. The epigenome includes heritable information such as DNA methylation. We hypothesized that the dietary supply of methyl donors would alter epigenetic reprogramming in sperm. This hypothesis was examined by feeding male mice a folate deficient (FD) and folate sufficient (FS) diets and then generating and analyzing DNA methylation profiles of their sperm. C57BL/6 males were fed either the FS or FD diet throughout life (FS, n=32; FD, n=35; 2-3 month old). Pooled gene promoter DNA methylation profiles were generated from the sperm of three FS males and four FD males using the method of MeDIP (Methylated DNA Immunoprecipitation) followed by microarray hybridization.

2013-11-02 | E-GEOD-52017 | biostudies-arrayexpress

Low paternal dietary folate alters the sperm epigenome and is associated with negative pregnancy outcomes

Project description:We hypothesized that the availability of folate, a soluble B vitamin, would alter the levels of DNA methylation in spermatogenesis with consequences for the sperm epigenome and pregnancy outcomes. We fed male mice with either a folate-deficient or a folate-sufficient diet throughout life. Males fed the folate-deficient diet had offspring with increased birth defects, which included craniofacial and musculoskeletal malformations. These phenotypes corresponded to developmental genes with altered methylation in sperm. To determine if there was transmission of epigenetic effects from sires to offspring, global gene expression levels were assessed in placenta from 18.5 dpc fetuses sired by either a folate-sufficient or folate-deficient male. Gene expression was measured in placenta of 18.5 dpc fetuses sired by either a folate sufficient male (n=4 placentas from different litters and different fathers) or a folate deficient (FD) male (n=4 placentas from different litters and different fathers).

2013-11-06 | E-GEOD-51819 | biostudies-arrayexpress

Low paternal dietary folate alters the sperm epigenome and is associated with negative pregnancy outcomes

2013-11-06 | GSE51819 | GEO

Impact of mothers' early life exposure to low or high folate on progeny outcome and DNA methylation patterns

Project description:The dynamic patterning of DNA and histone methylation during oocyte development presents a potentially susceptible time for epigenetic disruption due to early life environmental exposure of future mothers. We investigated whether maternal exposure to folic acid deficient (FD) and supplemented (FS) diets starting in utero could affect oocytes and cause adverse developmental and epigenetic effects in next generation progeny. Female BALB/c mice (F0) were placed on one of four amino acid defined diets for 4 weeks before pregnancy and throughout pregnancy and lactation: folic acid control (rodent daily recommended intake or DRI; Ctrl), 7−fold folic acid deficient (7FD), 10−fold folic acid supplemented (10FS) or 20−fold folic acid supplemented (20FS) diets. F1 female pups were weaned onto Ctrl diets, mated to produce the F2 generation, and the F2 offspring were examined at E18.5 for developmental and epigenetic abnormalities. Resorption was increased and litter sizes decreased amongst F2 E18.5 day litters in the 20FS group. Increases in abnormal embryo outcomes were observed in all three FD and FS groups. Subtle genome-wide DNA methylation alterations were found in the placentas and brains of F2 offspring in the 7D, 10FS and 20FS groups; in contrast, global and imprinted gene methylation were not affected. The findings show that early life female environmental exposures to both low and high folate prior to oocyte maturation can compromise oocyte quality, adversely affecting offspring of the next generation, in part by altering DNA methylation patterns.

2020-12-01 | GSE150629 | GEO

High-dose folic acid supplementation alters the human sperm methylome and is influenced by the MTHFR C677T polymorphism

Project description:Dietary folate is a major source of methyl groups required for DNA methylation, an epigenetic modification that is actively maintained and remodelled during spermatogenesis. While high dose folic acid supplementation (up to ten times the daily recommended dose) has been shown to improve sperm parameters in infertile men, the effects of supplementation on the sperm epigenome are unknown. To assess the impact of six months of high dose folic acid supplementation on the sperm epigenome, we studied 30 men with idiopathic infertility. Blood folate concentrations increased significantly after supplementation with no significant improvements in sperm parameters. Methylation levels of the differentially methylated regions of several imprinted loci (H19, DLK1/GTL2, MEST, SNRPN, PLAGL1, KCNQ1OT1) were normal both before and after supplementation. Reduced representation bisulfite sequencing (RRBS) revealed a significant global loss of methylation across different regions of the sperm genome. The most marked loss of DNA methylation was found in sperm from patients homozygous for the methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism, a common polymorphism in a key enzyme required for folate metabolism. RRBS analysis also showed that most of the differentially methylated tiles were located in DNA repeats, low CpG density and intergenic regions. Ingenuity Pathway Analysis revealed that methylation of promoter regions was altered in several genes involved in cancer and neurobehavioral disorders including CBFA2T3, PTPN6, COL18A1, ALDH2, UBE4B, ERBB2, GABRB3, CNTNAP4 and NIPA1. Our data reveal alterations of the human sperm epigenome associated with high dose folic acid supplementation, effects that were exacerbated by a common polymorphism in MTHFR. Reduced representation bisulfite sequencing of 28 human sperm samples before and after 6 month of high dose folic acid supplementation.

2015-09-10 | E-GEOD-72606 | biostudies-arrayexpress

Expression data from mouse intestine: BALB/c MTHFR+/+ on control diet vs BALB/c MTHFR+/- on folate deficient diet

Project description:Previous studies in our laboratory have shown that low folate diet (control diet with 2mg folate/kg, low folate diet with 0.3mg folate/kg) can induce intestinal tumors in BALB/c mice. We used microarrays to compare MTHFR+/+ BALB/c mice fed control diet and MTHFR+/- BALB/c mice fed low folate diet. After weaning, 4 BALB/c Mthfr +/+ mice were fed with a control diet (CD, 2mg folate/kg) and 4 BALB/c Mthfr +/- mice were fed a low folate diet (FD, 0.3mg folate/kg) for 1 year. Both diets contain succinylsulfanthiozole (1%) to prevent folate synthesis by intestine microbial biota.

2013-12-03 | E-GEOD-34011 | biostudies-arrayexpress

High-dose folic acid supplementation alters the human sperm methylome and is influenced by the MTHFR C677T polymorphism

2015-09-10 | GSE72606 | GEO

Paternal chronic folate supplementation induced transgenerational inheritance of acquired developmental and metabolic changes in chickens

Project description:Increasing evidence indicates that the paternal diet can result in offspring metabolic changes. A proposed mechanism for paternal transmission of environmental information is via the sperm noncoding RNAs, but the definite mechanism remains unclear in birds.

2018-11-21 | GSE122759 | GEO

Histone H3 lysine 4 trimethylation in sperm is transmitted to the embryo and associated with diet-induced phenotypes in the offspring

Project description:ChIP-Sequencing for H3K4me3 was performed on the sperm of individual mice fed a folate sufficient or folate deficient diet, and on a wildtype or KDM1A overexpressing transgenic background. Ultra-Low-Input ChIP-Sequencing was performed on 8-cell embryos from male wildtype mice fed a folate sufficient or folate deficient diet. We identified regions of the sperm epigenome that were sensitive to a folate deficient diet and found that multiple epigenetic stressors could cumulatively alter H3K4me3 in sperm. Additionally, we found that alterations in H3K4me3 levels in the sperm of folate deficient males were retained in the pre-implantation embryo. Finally, low-input RNA-Seq on 8-cell embryos from folate sufficient or folate deficient males on a wildtype or KDM1A transgenic background allowed us identify transcripts with deregulated gene expression in the pre-implantation embryo. Regulating promoters with aberrant transcription in the 8-cell embryos overlapped promoters with altered H3K4me3 in sperm.

2021-02-18 | GSE135678 | GEO

Maternal folate and newborn DNA methylation meta-analysis

Project description:<p>Folic acid is routinely recommended for women trying to conceive to ensure proper fetal development. Mechanisms whereby periconceptional folate influences normal development and disease are poorly understood: epigenetics may be involved. This data represents meta-analysis results from a large epigenomics study to examine the association between maternal plasma folate during pregnancy and epigenome-wide DNA methylation using Illumina's HumanMethyl450 (450K) Beadchip in 1,996 newborns from two European cohorts. Results for all CpGs analyzed (419,905) are provided. </p> <p>These data may be downloaded through the dbGaP Authorized Access portal under phg000701.v1.</p>

| phs001059 | dbGaP

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