Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptomics of rat born to dams fed a diet deficient in methyl group donors

ABSTRACT: It is clearly established that the maternal diet during pregnancy can induce physiological and metabolic adaptations in the developing fetus which determine its susceptibility later in life to develop diabetes, obesity... The molecular and genomic mechanisms underlying the programming of the metabolic syndrome remain largely unknown but may involve resetting of epigenetic marks and fetal gene expression. We analyzed the profile of the liver transcriptome in 21-day-old rats born to mothers fed with a standard diet or a diet lacking methyl donor nutrients (Vitamin B12 and folates) during gestation and lactation. From a total of 44,000 probes for 26,456 genes, we found two gene clusters whose expression levels had statistically significant differences between control and deficient rats: 3,269 up-regulated and 2,841 down-regulated genes. Bioinformatics analysis revealed that these genes are mainly involved in glucose and lipid metabolism, nervous system, coagulation, endoplasmic reticulum (ER) stress and mitochondrial function. Modifications of gene expression in rat liver were measured in 21-day-old rats born to mothers fed with a standard diet or a diet lacking methyl donor nutrients (Vitamin B12 and folates). Eight independent experiments were performed (4 Controls versus 4 Methyl Donor Deficiency - MDD).

ORGANISM(S): Rattus norvegicus

SUBMITTER: Sebastien Hergalant

PROVIDER: E-GEOD-59039 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Identification of master genes involved in liver key functions through transcriptomics and epigenomics of methyl donor deficiency in rat: relevance to nonalcoholic liver disease.

Chen Gaili G Broséus Julien J Hergalant Sébastien S Donnart Audrey A Chevalier Catherine C Bolaños-Jiménez Francisco F Guéant Jean-Louis JL Houlgatte Rémi R

Molecular nutrition & food research 20141209 2

<h4>Scope</h4>Our study aims to investigate molecular events associated to methyl donor deficiency (MDD) by analyzing the transcriptome and the methylome of MDD rats in liver.<h4>Methods and results</h4>Twenty-one-day-old rats born to mothers fed either with a standard diet or a MDD diet during gestation and lactation were compared. From a total of 44 000 probes for 26 456 genes, we found two gene clusters in MDD rats whose expression levels had significant differences compared with controls: 32 ...[more]

PMID: 25380481

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Project description:BACKGROUND & AIMS: Inflammatory Bowel Diseases (IBD), including Crohnâ??s disease and ulcerative colitis, are chronic illnesses that are thought to develop secondary to a pathologic interaction between the immune system and the intestinal microflora that is manifested by the gut mucosa. IBD has been recognized as disorders in which developmental epigenetic changes, such as DNA methylation, may play an important pathogenic role. DNA methylation can be influenced in mammals by dietary exposures. A methyl-donor diet has been specifically found to be effective in inducing permanent changes in DNA methylation at certain genomic loci in murine models. Importantly, the methyl-donor substances utilized are routinely incorporated into prenatal micronutrient supplements for humans. In this study we addressed whether maternal exposure to a methyl-donor diet induces prolonged alterations in offspring colitis susceptibility and whether it leads to stable colonic mucosal epigenetic changes and gene expression alterations in mice. We also assessed whether the maternal methyl-donor diet induced persistent changes in the colonic microbiota in the offspring. METHODS: Colonic mucosa from offspring of mothers fed a methyl donor diet (MD) or control diet was interrogated by methylation specific amplification microarray (MSAM) at postnatal day 30 (P30) and P90 to screen for changes in DNA methylation, with bisulfite pyrosequencing validation. Transcriptomic changes in the same tissue were analyzed by microarray expression profiling and real time RT-PCR. The mucosal microbiome was studied by high throughput, detailed pyrosequencing of 16S rRNA. RESULTS: MD exposure during prenatal and early development lead to a significant increase in colitis susceptibility that persisted even after 69 days of diet reversal (P90). MD exposure also influenced DNA methylation and expression at select genomic loci. Overlap between DNA methylation and gene expression changes was confirmed at Ppara, a gene previously implicated in murine colitis. Metagenomic analyses failed to reveal consistent bacteriomic differences between the P30 and P90 age groups. CONCLUSIONS: Prenatal and early developmental exposure to MD induces increased colitis susceptibility, mucosal epigenomic, and transcriptomic changes that do not appear to associate with consistent microbiomic alterations. These findings underscore the importance of maternal nutrition on offspring colitis susceptibility in mammals and implicate the importance of the associated mucosal epigenetic modification. Our results bare potentially significant public health relevance as well. 4 independent MD versus control comparisons at P90 were performed as follows. RNA (0.4ug) samples were processed and labelled with Cy3 and Cy5 (Quick Amp labelling kit, two color, Agilent technologies) and 4 independent P90 MD to P90 control comparisons were done on Agilent technologies 4x44k whole genomic expression microarray G2519F, Amadid:014868)

Dataset Information

Transcriptomics of rat born to dams fed a diet deficient in methyl group donors

Publications

Identification of master genes involved in liver key functions through transcriptomics and epigenomics of methyl donor deficiency in rat: relevance to nonalcoholic liver disease.

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