Choline is an essential nutrient. Large amounts of choline are delivered across the placenta to the developing fetus, contributing to brain development and, consequently, affecting memory performance during adulthood. Rodent studies have described specific epigenetic mechanisms, whereby choline deprivation altered the neurobiology of progenitor cells, modifying their proliferation and survival. Choline, via oxidation to betaine, provides one-carbon units to the methionine cycle and further, to all methylation processes part of the epigenetic control. We found that the choline dehydrogenase (Chdh) gene, responsible for this conversion, is expressed in the brain of adult and fetal mice. By deleting the Chdh gene, we investigated the effects of low betaine synthesis on fetal brain development. We assessed cell proliferation in Chdh+/+ and Chdh-/- fetuses at embryonic day 17 (E17) by immunohistochemistry. Mitosis and apoptosis were not significantly altered by fetal genotype. Further studies will be needed to establish if gene-specific methylation is altered between Chdh wildtype and knockout mice fetuses.Master of Scienc
