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Metabolomic and Transcriptomic Signatures of Prenatal Excessive Methionine in Mice

ABSTRACT: Micronutrients are key regulators of prenatal one-carbon (C1) metabolism. We show here that prenatal excessive methionine (MET), a principal micronutrient and methyl-donor, produces in early life stages significant changes in the components of brain C1 pathways and other metabolic pathways including glutamate transmission, mitochondrial function, and lipid metabolism.

ORGANISM(S): Mouse Mus Musculus

TISSUE(S): Brain

SUBMITTER: Siwei Chen

PROVIDER: ST001413 | MetabolomicsWorkbench | Wed Jun 24 00:00:00 BST 2020

REPOSITORIES: MetabolomicsWorkbench

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Metabolomic and Transcriptomic Signatures of Prenatal Excessive Methionine in Mice Support Nature Rather than Nurture in the Pathogenesis and Therapy of Schizophrenia

Project description:Abstract: The imbalance of prenatal micronutrients may perturb one-carbon (C1) metabolism and increase the risk for neuropsychiatric disorders. Prenatal excessive methionine (MET) produces in mice behavioral phenotypes reminiscent of human schizophrenia. Whether in-utero programming or early life caregiving mediate these effects is, however, unknown. Here, we show that the behavioral deficits of MET are independent of the early life mother-infant interaction. We also show that MET produces in early life profound changes in the brain C1 pathway components as well as glutamate transmission, mitochondrial function, and lipid metabolism. Bioinformatics analysis integrating metabolomics and transcriptomic data reveal dysregulations of glutamate transmission and lipid metabolism, and identify perturbed pathways of methylation and redox reactions. Our transcriptomics Linkage analysis of MET mice and schizophrenia subjects reveals master genes involved in inflammation and myelination. Finally, we identify potential metabolites as early biomarkers for neurodevelopmental defects and suggest new therapeutic targets for schizophrenia.

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