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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Identify acetylation marks from embryonic calvaria cell gene promoter regions from maternal high fat or control diet dams using H3K27ac ChIP-Seq.

ABSTRACT: Genes with increased H3K27ac marks in their promoters were found in mice embryonic calvaria cells using H3K27ac ChIP-Seq. Recent data suggests that in animals and humans that a maternal diet high in fat leads to poor bone growth and development in offspring. Genes with increased H3K27ac epigenetic marks normally have higher levels of expression. Understanding which genes are being upregulated in the offspring due to maternal diet would allow for better treatments to combat bone loss to be developed.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Mus musculus musculus

SUBMITTER: Perry Caviness

PROVIDER: E-MTAB-11712 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Identify trimethylation marks from embryonic calvaria cell gene promoter regions from maternal high fat or control diet dams using H3K27me3 ChIP-Seq.

Project description:Genes with increased H3K27me3 marks in their promoters were found in mice embryonic calvaria cells using H3K27me3 ChIP-Seq. Recent data suggests that in animals and humans that a maternal diet high in fat leads to poor bone growth and development in offspring. Genes with increased H3K27me3 epigenetic marks normally have lower levels of expression. Understanding which genes are being downregulated in the offspring due to maternal diet would allow for better treatments to combat bone loss to be developed.

2022-05-31 | E-MTAB-11713 | biostudies-arrayexpress

Identify acetylation marks in adult mouse L4 vertebrae gene promoter regions from maternal high fat diet dams using H3K27ac ChIP-Seq

Project description:Genes with increased H3K27ac marks in their promoters were found in adult mice L4 vertebrae from mice using H3K27ac ChIP-Seq. Recent data suggests that in animals and humans that a maternal diet high in fat leads to poor bone growth and development in offspring. Genes with increased H3K27ac epigenetic marks normally have higher levels of expression. Understanding which genes are being upregulated due to maternal or offspring high fat diet would allow for better treatments to combat bone loss to be developed.

2022-05-31 | E-MTAB-11718 | biostudies-arrayexpress

DNA methylation alternations in the offspring adipose from chromium restriction diet dams

Project description:Maternal chromium restriction may disturb susceptibility in offspring. Adipose from maternal chromium diet has 1214 CpG sites that exhibit differential DNA methylationregulated compared to control. We performed DNA methylation array analyses of offspring adipose from chromium restriction dams and control diet dams at 32 week (n=3 per group).

2016-09-08 | E-GEOD-82030 | biostudies-arrayexpress

Maternal Nutrition Induces Pervasive Gene Expression Changes but no Detectable DNA Methylation Differences in the Liver of Adult Offspring [RRBS]

Project description:Aims: Epidemiological and animal studies have shown that maternal diet can influence metabolism in adult offspring. However, the molecular mechanisms underlying these changes remain poorly understood. Here, we aim to explore phenotypes induced by maternal obesity in a mouse model and examine gene expression and epigenetic alterations in adulthood induced by maternal diet. Methods: We analyzed genetically identical male mice born from dams fed a high- or low-fat diet throughout pregnancy and until day 21 postpartum. After weaning, half of the males of each group were fed a high-fat diet, the other half a low-fat diet. We first characterized the genome-wide gene expression patterns of six tissues of adult offspring - liver, pancreas, white adipose, brain, muscle and heart [GSE40903] . We then measured DNA methylation patterns in liver at selected loci and throughout the genome. Results: Maternal diet had a significant effect on the body weight of the offspring when they are fed an obesogenic diet after weaning. Our analyses showed that maternal diet had a pervasive effect on gene expression, with a pronounced effect in liver where it affected many genes involved in inflammation, cholesterol synthesis and RXR activation. Maternal diet had no detectable effect on DNA methylation in the liver. Conclusions: Overall, our findings highlighted the persistent influence of maternal diet on adult tissue regulation and suggested that the transcriptional changes were unlikely to be caused by DNA methylation differences in adult liver. Methylation is compared between nine week old animals fed a common diet as adults, but derived from mothers fed different diets.

2014-03-04 | E-GEOD-52266 | biostudies-arrayexpress

Maternal Nutrition Induces Pervasive Gene Expression Changes but no Detectable DNA Methylation Differences in the Liver of Adult Offspring [selected loci]

2014-03-04 | E-GEOD-52267 | biostudies-arrayexpress

Are you also what Your Mother Eats? Distinct Proteomic Portrait as a Result of Maternal High-Fat Diet in the Cerebral Cortex of the Adult Mouse.

Project description:Background: Epidemiological studies suggest an association between maternal obesity and adverse neurodevelopmental outcomes in offspring. Objective: To compare the global proteomic portrait in the cerebral cortex between mice born to mothers on a high-fat or control diet who themselves were fed a high-fat or control diet. Methods: Male mice born to dams fed a control (C) or high fat (H) diet four weeks before conception and during gestation and lactation were assigned to either C or H diet at weaning. Mice (n=24) were sacrificed at 19-weeks and their cerebral cortices were pooled into 8 samples and analysed using an iTRAQ based 2D LC-MS methodology. Results: A total of 6,695 proteins were identified and fully quantified (q<0.01). Approximately 10% of these proteins demonstrated a minimum of one Standard Deviation of regulation across all biological replicates in at least one of the experimental groups (CH, HC, HH) relative to the control (CC). Principal component analysis and hierarchical clustering analysis showed that mice clustered based on the diet of the mother and not their current diet. In silico bioinformatics analysis revealed that maternal high-fat diet was significantly associated with response to hypoxia/oxidative stress and apoptosis in the cerebral cortex of the adult offspring. Conclusion: Maternal high-fat diet was associated with distinct endophenotypic changes of the adult mouse cerebral cortex independent of the diet of the offspring. The identified modulated proteins could represent novel therapeutic targets for the prevention of neuropathological features resulting from maternal obesity.

2018-01-29 | PXD001540 | Pride

Maternal Undernutrition Results in Transcript Changes in Male Offspring that May Promote Resistance to High Fat Diet Induced Weight Gain

Project description:Maternal nutrition during embryonic development and lactation influences multiple aspects of offspring health. Using mice, this study investigates the effects of maternal caloric restriction (CR) during mid-gestation and lactation on offspring neonatal development and on adult metabolic function when challenged by a high fat diet (HFD). The CR maternal model produced male and female offspring that were significantly smaller, in terms of weight and length, and females had delayed puberty. Adult offspring born to CR dams had a sexually dimorphic response to the high fat diet. Compared to offspring of maternal control dams, adult female, but not male, CR offspring gained more weight in response to high fat diet at 10 weeks. In adipose tissue of male HFD offspring, maternal undernutrition resulted in blunted expression of genes associated with weight gain and increased expression of genes that protect against weight gain. Regardless of maternal nutrition status, HFD male offspring showed increased expression of genes associated with nonalcoholic liver disease (NAFLD). Furthermore, we observed significant, sexually dimorphic differences in serum TSH. These data reveal tissue- and sex-specific changes in gene and hormone regulation following mild maternal undernutrition, which may offer protection against diet induced weight gain in adult male offspring.

2024-01-04 | GSE247985 | GEO

Multi-omics data integration reveals sex-dependent hippocampal programming by maternal high-fat diet during lactation in adult mouse offspring

Project description:Early-life exposure to high-fat diet (HF) can program metabolic and cognitive alterations in adult offspring. Although the hippocampus plays a crucial role in memory and metabolic homeostasis, few studies reported the impact of maternal HF on this structure. We assessed the effects of maternal HF during lactation on physiological, metabolic and cognitive parameters in young adult offspring mice. To identify early-programming mechanisms in hippocampus, we developed a multi-omics strategy in male and female offspring. Maternal HF induced a transient increased body weight at weaning, a mild glucose intolerance only in 3-month-old male mice with no change in plasma metabolic parameters in adult male and female offspring. Behavioral alterations revealed by Barnes maze test were observed both in 6-month-old male and female mice. Multi-omics strategy unveiled sex-specific transcriptomic and proteomic modifications in the hippocampus of adult offspring. These studies, that were confirmed by regulon analysis, showing that, although genes whose expression was modified by maternal HF were different between sexes, the main pathways affected were similar with mitochondria and synapses as main hippocampal targets of maternal HF. The effects of maternal HF reported here may help to better characterize sex-dependent molecular pathways involved in cognitive disorders and neurodegenerative diseases.

2024-01-26 | PXD045639 | Pride

Maternal Smchd1 regulates Hox gene expression and patterning in the mouse embryo [ESC RRBS]

Project description:Parents transmit genetic and epigenetic information to their offspring. Maternal effect genes regulate the offspring epigenome to ensure normal development. Here we report that the epigenetic regulator SMCHD1 has a maternal effect on Hox gene expression and skeletal patterning. Maternal SMCHD1, present in the oocyte and preimplantation embryo, prevents precocious activation of Hox genes post-implantation. Without maternal SMCHD1, highly penetrant posterior homeotic transformations occur in the embryo. Hox genes are decorated with Polycomb marks H2AK119ub and H3K27me3 from the oocyte throughout early embryonic development; however, loss of maternal SMCHD1 does not deplete these marks. Therefore, we propose maternal SMCHD1 acts downstream of Polycomb marks to establish a chromatin state necessary for persistent epigenetic silencing and appropriate Hox gene expression later in the developing embryo. This is a striking role for maternal SMCHD1 in long-lived epigenetic effects impacting offspring phenotype.

2022-06-27 | GSE203617 | GEO

Maternal Smchd1 regulates Hox gene expression and patterning in the mouse embryo [H2AK119ub CUT&RUN]

2022-06-27 | GSE183739 | GEO

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