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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE34011 | GEO | 2013/12/03

SECONDARY ACCESSION(S): PRJNA150595

REPOSITORIES: GEO

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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

Expression data from mouse intestine: C57Bl/6 MTHFR+/- vs BALB/c MTHFR+/-

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. In addition, we reported that C57Bl/6J mice did not form tumors under the same conditions. We used microarrays to identify the genetic differences between BALB/c and C57Bl/6J mice that promote tumorigenesis in BALB/c mice. Two groups of mice will be used in the micro-array experiment. One group will consist of four BALB/c mice and the second group will consist of four C57Bl/6 mice. Both groups have mild MTHFR deficiency (Mthfr+/-) and will receive low folate diet (0.3 mg folate/kg) for one year. RNA samples will be extracted from duodenum, the first section of the small intestine where tumors were observed in BALB/c mice. Eight Affymetrix GeneChip Mouse Gene 1.0 ST Array Chips will be used in this experiment.

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Expression data from mouse intestine: C57Bl/6 MTHFR+/- vs BALB/c MTHFR+/-

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Testicular MTHFR deficiency may explain sperm DNA hypomethylation associated with high dose folic acid supplementation

Project description:Supplementation with high doses of folic acid, an important mediator of one-carbon transfers for DNA methylation, is used clinically to improve sperm parameters in infertile men. We recently detected an unexpected loss of DNA methylation in the sperm of idiopathic infertile men after 6 months of daily supplementation with 5mg folic acid (>10× the daily recommended intake-DRI), exacerbated in men homozygous for a common variant in the gene encoding an important enzyme in folate metabolism, methylenetetrahydrofolate reductase (MTHFR 677C>T). To investigate the epigenomic impact and mechanism underlying effects of folic acid on male germ cells, wildtype and heterozygote mice for a targeted inactivation of the Mthfr gene were fed high-dose folic acid (10× the DRI) or control diets for six months. No changes were detected in general health, sperm counts or methylation of imprinted genes. Reduced representation bisulfite sequencing revealed sperm DNA hypomethylation in Mthfr+/- mice on the 10× diets. Wildtype mice demonstrated sperm hypomethylation only with a very high dose (20×) of folic acid for 12 months. Testicular MTHFR protein levels decreased significantly in wildtype mice on the 20× diet but not in those on the 10× diet, suggesting a possible role for MTHFR deficiency in sperm DNA hypomethylation. In-depth analysis of the folic acid-exposed sperm DNA methylome suggested mouse/human susceptibility of sequences with potential importance to germ cell and embryo development. Our data provide evidence for a similar cross-species response to high dose folic acid supplementation, of sperm DNA hypomethylation, and implicate MTHFR downregulation as a possible mechanism.

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Transcription profiling of blood cells from rats fed a folate deficient diet vs fed a normal diet for 28 days

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Sperm DNA methylation defects in a new mouse model of the 5,10-methylenetetrahydrofolate reductase 677C>T variant and correction with moderate dose folic acid supplementation.

Project description:5,10-Methylenetetrahydrofolate reductase (MTHFR) is an enzyme that plays a key role in providing methyl groups for DNA methylation, including during spermatogenesis. A common genetic variant in humans (MTHFR 677C>T), results in reduced enzyme activity and has been linked to various disorders, including male infertility. A new animal model has been created by reproducing the human equivalent of the polymorphism in mice using CRISPR/Cas9. Biochemical parameters in the Mthfr 677TT mice recapitulate alterations found in MTHFR 677TT men. Our aims were to: 1) characterize the sperm DNA methylome of the Mthfr 677CC and TT mice on a control diet (2mg folic acid/kg diet) and 2) assess the effects of folic acid deficiency (0.3mg/kg diet) and supplementation (10 mg/kg diet) on the sperm DNA methylome. Body and reproductive organ weights, testicular sperm counts, and histology were examined. DNA methylation in sperm was assessed using bisulfite pyrosequencing, Illumina Mouse Methylation Array and whole genome bisulfite sequencing. Reproductive parameters and imprinted gene methylation were unaffected by genotype or diets. The largest effect was due to genotype, with sperm from 677TT mice showing more hypo- than hypermethylation. Folate-deficient diets resulted in sperm hyper- and hypomethylation in CC and TT mice. Folic acid supplementation caused mostly hypermethylation in sperm of males of both genotypes and was found to partially correct the DNA methylation alterations in sperm associated with the TT genotype. The new mouse model will be useful in understanding the role of MTHFR deficiency in male fertility and in designing folate supplementation regimens for the clinic.

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Mus musculus

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

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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.

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Project description:5, 10-Methylenetetrahydrofolate reductase (MTHFR) is a crucial enzyme in the folate metabolic pathway with a key role in generating methyl groups. As MTHFR deficiency impacts male fertility and sperm DNA methylation, there is the potential for epimutations to be passed to the next generation. Here, we assessed whether the impact of MTHFR deficiency on testis morphology and sperm DNA methylation is exacerbated across generations. While MTHFR deficiency in F1 fathers has only minor effects on sperm counts and testis weights and histology, F2 generation sons show further deterioration in reproductive parameters. Extensive loss of DNA methylation is observed in both F1 and F2 sperm, with >80% of sites shared between generations, suggestive of regions consistently susceptible to MTHFR deficiency. These regions are generally methylated during late prenatal germ cell development and are enriched in young retrotransposons. As retrotransposons are resistant to reprogramming of DNA methylation in prenatal germ cells, their hypomethylated state in the sperm of F1 males could contribute to the worsening reproductive phenotype observed in F2 MTHFR- deficient males, findings compatible with the intergenerational passage of epimutations.

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