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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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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.

ABSTRACT: 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.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Mus musculus

SUBMITTER: Perry Caviness

PROVIDER: E-MTAB-11713 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

Project description: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.

2022-05-31 | E-MTAB-11712 | 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.

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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.

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

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

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

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