ArticleThe American journal of clinical nutrition2012
Dietary folate, but not choline, modifies neural tube defect risk in Shmt1 knockout mice.
Article in The American journal of clinical nutrition, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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28 citing papers in PubMed, 54 citations in OpenAlex.
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- Prenatal Intake of High Multivitamins or Folic Acid With or Without Choline Contributes to Gut Microbiota-Associated Dysregulation of Serotonin in Offspring.Molecular nutrition & food research · 2025Article
- DTYMK is an essential gene in mice and heterozygosity does not cause neural tube defects.Archives of biochemistry and biophysics · 2024Article
- Micronutrient regulation of the DNA methylome.Frontiers in epigenetics and epigenomics · 2024Review
- Modification of the serotonergic systems and phenotypes by gestational micronutrients.The Journal of endocrinology · 2023Article
- Reduced methionine synthase expression results in uracil accumulation in mitochondrial DNA and impaired oxidative capacity.PNAS nexus · 2023Article
- A quest for genetic causes underlying signaling pathways associated with neural tube defects.Frontiers in pediatrics · 2023Review
- Folate, Vitamin B12, and Homocysteine Levels in Women With Neural Tube Defect-Affected Pregnancy in Addis Ababa, Ethiopia.Frontiers in nutrition · 2022Article
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- Identification of Novel Variants in Cleft Palate-Associated Genes in Brazilian Patients With Non-syndromic Cleft Palate Only.Frontiers in cell and developmental biology · 2021Article
- Variations in maternal vitamin A intake modifies phenotypes in a mouse model of 22q11.2 deletion syndrome.Birth defects research · 2020Article
- Up-regulation of RNA Binding Proteins Contributes to Folate Deficiency-Induced Neural Crest Cells Dysfunction.International journal of biological sciences · 2020Article
- Cytosolic 10-formyltetrahydrofolate dehydrogenase regulates glycine metabolism in mouse liver.Scientific reports · 2019Article
- The Role of Single-Nucleotide Polymorphisms in the Function of Candidate Tumor Suppressor ALDH1L1.Frontiers in genetics · 2019Review
- Nuclear Folate Metabolism.Annual review of nutrition · 2018Review
- A hybrid stochastic model of folate-mediated one-carbon metabolism: Effect of the common C677T MTHFR variant on de novo thymidylate biosynthesis.Scientific reports · 2017Article
- Metabolic interactions with cancer epigenetics.Molecular aspects of medicine · 2017Review
- The Roles of SUMO in Metabolic Regulation.Advances in experimental medicine and biology · 2017Review
- Article
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6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundLow dietary choline intake has been proposed to increase the risk of neural tube defects (NTDs) in human populations. Mice with reduced Shmt1 expression exhibit a higher frequency of NTDs when placed on a folate- and choline-deficient diet and may represent a model of human NTDs. The individual contribution of dietary folate and choline deficiency to NTD incidence in this mouse model is not known.
objectiveTo dissociate the effects of dietary folate and choline deficiency on Shmt1-related NTD sensitivity, we determined NTD incidence in embryos from Shmt1-null dams fed diets deficient in either folate or choline.
designShmt1(+/+) and Shmt1(-/-) dams were maintained on a standard AIN93G diet (Dyets), an AIN93G diet lacking folate (FD), or an AIN93G diet lacking choline (CD). Virgin Shmt1(+/+) and Shmt1(-/-) dams were crossed with Shmt1(+/-) males, and embryos were examined for the presence of NTDs at embryonic day (E) 11.5 or E12.5.
resultsExencephaly was observed only in Shmt1(-/-) embryos isolated from dams maintained on the FD diet (P = 0.004). Approximately 33% of Shmt1(-/-)embryos (n = 18) isolated from dams maintained on the FD diet exhibited exencephaly. NTDs were not observed in any embryos isolated from dams maintained on the CD (n = 100) or control (n = 152) diets or in any Shmt1(+/+) (n = 78) or Shmt1(+/-) embryos (n = 182).
conclusionMaternal folate deficiency alone is sufficient to induce NTDs in response to embryonic Shmt1 disruption.
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