Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA157531 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression profiles of normal colons in ApcMin mice that were fed methyl deficient diet for 11 weeks vs controls Expression profiles of normal colons in ApcMin mice that were fed methyl deficient diet for 11 weeks vs controls fed methyl donor sufficient diets
2012-04-30 | E-GEOD-37010 | biostudies-arrayexpress
Project description:Expression profiles of normal colons in ApcMin mice that were fed methyl deficient diet for 11 weeks vs controls
2012-05-01 | GSE37010 | GEO
Project description:The metabolic pathways that underlie the association between folate deficiency and increased risk for colorectal cancer (CRC) remain unclear. We have studied the effect of C1THF synthase (encoded by the Mthfd1 gene) and dietary folate and choline on intestinal tumor development in Apcmin/+ mice and azoxymethane (AOM)-induced colon cancer in mice. Mthfd1 deficiency did not alter tumor number or load in Apcmin/+ mice, but did result in a decreased incidence of colon tumors. Conversely, Mthfd1 deficiency increased tumor number 3.5-fold and tumor load 2-fold in AOM-treated mice. Here we tested colons isolated from wildtype and Mthfd1-deficient animals for alterations in gene expression. Keywords: genetic modification RNA was isolated from proximal colons of MTHFD heterozygous and wild-type mice raised on a control diet. Three colon samples were isolated from each genotype to provide biological replication.
2010-03-20 | E-GEOD-15419 | biostudies-arrayexpress
Project description:The metabolic pathways that underlie the association between folate deficiency and increased risk for colorectal cancer (CRC) remain unclear. We have studied the effect of C1THF synthase (encoded by the Mthfd1 gene) and dietary folate and choline on intestinal tumor development in Apcmin/+ mice and azoxymethane (AOM)-induced colon cancer in mice. Mthfd1 deficiency did not alter tumor number or load in Apcmin/+ mice, but did result in a decreased incidence of colon tumors. Conversely, Mthfd1 deficiency increased tumor number 3.5-fold and tumor load 2-fold in AOM-treated mice. Here we tested colons isolated from wildtype and Mthfd1-deficient animals for alterations in gene expression. Keywords: genetic modification
2010-03-20 | GSE15419 | GEO
Project description:Evaluation of transgenerational influence of paternal dietary methyl substrates on offspring and grand-offspring brain and behavior Dietary intake of methyl donors, such as folic acid and methionine, shows considerable intra-individual variation in human populations. While it is recognized that maternal departures from the optimum of dietary methyl donor intake can increase the risk for mental health issues and neurological disorders in offspring, it has not been explored whether paternal dietary methyl donor intake influences behavioral and cognitive functions in the next generation. Here, we report that elevated paternal dietary methyl donor intake in a mouse model, transiently applied prior to mating, resulted in offspring animals (MD F1 mice) with deficits in hippocampus-dependent learning and memory, impaired hippocampal synaptic plasticity and reduced hippocampal theta oscillations. Gene expression analyses revealed altered expression of the methionine adenosyltransferase Mat2a and BK channel subunit Kcnmb2, which was associated with changes in Kcnmb2 promoter methylation in MD F1 mice. These phenomena did not extend into the F2 offspring generation. Together, our data indicate that paternal dietary factors influence cognitive and neural functions in the offspring generation.
2017-04-20 | GSE90499 | GEO
Project description:Evaluation of transgenerational influence of paternal dietary methyl substrates on offspring and grand-offspring brain and behavior Dietary intake of methyl donors, such as folic acid and methionine, shows considerable intra-individual variation in human populations. While it is recognized that maternal departures from the optimum of dietary methyl donor intake can increase the risk for mental health issues and neurological disorders in offspring, it has not been explored whether paternal dietary methyl donor intake influences behavioral and cognitive functions in the next generation. Here, we report that elevated paternal dietary methyl donor intake in a mouse model, transiently applied prior to mating, resulted in offspring animals (MD F1 mice) with deficits in hippocampus-dependent learning and memory, impaired hippocampal synaptic plasticity and reduced hippocampal theta oscillations. Gene expression analyses revealed altered expression of the methionine adenosyltransferase Mat2a and BK channel subunit Kcnmb2, which was associated with changes in Kcnmb2 promoter methylation in MD F1 mice. These phenomena did not extend into the F2 offspring generation. Together, our data indicate that paternal dietary factors influence cognitive and neural functions in the offspring generation.
2017-04-20 | GSE90158 | GEO
Project description:BALB/c and CBA/Ca male mice were maintained for 8 weeks on a synthetic diet lacking in choline and folic acid and sacrificed after the end of dietary restrictions. The design of this study is further described in Voutounou, M., C .D. Glen, and Y. E. 2012. The effects of methyl-donor deficiency on mutation induction and transgenerational instability in mice. Mutat. Res. 734(1):1-4 (PMID: 22569175) The pattern of gene expression in spleen of mice sacrificed immediatelly after the end of dietary restrictions is not significatly altered.
2014-05-29 | GSE57521 | GEO
Project description:BALB/c male mice were maintained for 8 weeks on a synthetic diet lacking in choline and folic acid and sacrificed 0, 2 and 6 weeks after the end of dietary restrictions. The design of this study is further described in Voutounou, M., C .D. Glen, and Y. E. 2012. The effects of methyl-donor deficiency on mutation induction and transgenerational instability in mice. Mutat. Res. 734(1):1-4 (PMID: 22569175) The pattern of gene expression in liver and kidney of mice sacrificed immediatelly after the end of dietary restrictions is significatly altered.
2012-12-13 | GSE42744 | GEO
Project description:CBA/Ca male mice were maintained for 8 weeks on a synthetic diet lacking in choline and folic acid and sacrificed 0 and 2 weeks after the end of dietary restrictions. The design of this study is further described in Voutounou, M., C .D. Glen, and Y. E. 2012. The effects of methyl-donor deficiency on mutation induction and transgenerational instability in mice. Mutat. Res. 734(1):1-4 (PMID: 22569175) The pattern of gene expression in liver of mice sacrificed immediatelly after the end of dietary restrictions is significatly altered.
2014-05-29 | GSE57523 | GEO
Project description:Abstract: Choline is an essential nutrient and methyl donor required for epigenetic regulation. Here, we assess the impact of gut microbial choline metabolism on bacterial fitness and host biology by engineering a microbial community to lack a single choline-utilizing enzyme. Our results indicate that choline-utilizing bacteria compete with the host for this nutrient, significantly impacting plasma and hepatic levels of methyl-donor metabolites recapitulating biochemical signatures of choline deficiency. Mice harboring high levels of choline-consuming bacteria show increased susceptibility to metabolic disease. Furthermore, bacterially-induced reduction of methyl-donor availability alters global DNA methylation patterns in both adult mice and their offspring in utero and engenders anxious behavior. Altogether, our results reveal an underappreciated aspect of bacterial choline metabolism (i.e., methyl-donor depletion) that is linked to alterations in metabolism, epigenetics, and behavior. More broadly, this work suggests that interpersonal differences in microbial metabolism should be considered when determining optimal levels of nutrient intake.
2017-07-28 | GSE100983 | GEO