Summary of Study ST003211

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR002002. The data can be accessed directly via it's Project DOI: 10.21228/M8TR5T This work is supported by NIH grant, U2C- DK119886.

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This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST003211
Study TitleFetal growth delay caused by loss of non-canonical imprinting is resolved late in pregnancy and culminates in offspring overgrowth
Study SummaryGermline epigenetic programming, including genomic imprinting, substantially influences offspring development. Polycomb Repressive Complex 2 (PRC2) plays an important role in Histone 3 Lysine 27 trimethylation (H3K27me3)-dependent imprinting, loss of which leads to growth and developmental changes in mouse offspring. In this study, we show that offspring from mouse oocytes lacking the PRC2 protein Embryonic Ectoderm Development (EED) were initially developmentally delayed, characterised by low blastocyst cell counts and substantial growth delay in mid-gestation embryos. This initial developmental delay was resolved as offspring underwent accelerated fetal development and growth in late gestation resulting in offspring that were similar stage and weight to controls at birth. The accelerated development and growth in offspring from Eed-null oocytes was associated with remodelling of the placenta, which involved an increase in fetal and maternal tissue size, conspicuous expansion of the glycogen enriched cell population and delayed parturition. Despite placental remodelling and accelerated offspring fetal growth and development, placental efficiency and fetal blood glucose levels were low, and the fetal blood metabolome was unchanged. Moreover, while expression of the H3K27me3-imprinted gene and amino acid transporter Slc38a4 was increased, fetal blood levels of individual amino acids were similar to controls, indicating that placental amino acid transport was not enhanced. Genome-wide analyses identified extensive transcriptional dysregulation and DNA methylation changes in affected placentas, including a range of imprinted and non-imprinted genes. Together, while deletion of Eed in growing oocytes resulted in fetal growth and developmental delay and placental hyperplasia, our data indicate a remarkable capacity for offspring fetal growth to be normalised despite inefficient placental function and the loss of H3K27me3-dependent genomic imprinting.
Institute
Hudson Institute of Medical Research
DepartmentCentre for Reproductive Health
Last NameWestern
First NamePatrick
Address27–31 Wright Street Clayton VIC 3168
Emailpatrick.western@hudson.org.au
Phone+61 3 8572 2700
Submit Date2024-05-15
Raw Data AvailableYes
Raw Data File Type(s)mzXML
Analysis Type DetailGC-MS
Release Date2024-05-22
Release Version1
Patrick Western Patrick Western
https://dx.doi.org/10.21228/M8TR5T
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Factors:

Subject type: Mammal; Subject species: Mus musculus (Factor headings shown in green)

mb_sample_id local_sample_id Sample source Genotype
SA3516062703cardiac blood HET
SA3516072714cardiac blood HET
SA3516082665cardiac blood HET
SA3516092645cardiac blood HET
SA3516102795cardiac blood HET
SA3516112789cardiac blood HET
SA3516122785cardiac blood HET
SA3516132730cardiac blood HET
SA3516142757cardiac blood HET
SA3516152716cardiac blood HOM
SA3516162729cardiac blood HOM
SA3516172740cardiac blood HOM
SA3516182748cardiac blood HOM
SA3516192721cardiac blood HOM
SA3516202763cardiac blood HOM
SA3516212775cardiac blood HOM
SA3516222684cardiac blood WT
SA3516232738cardiac blood WT
SA3516242732cardiac blood WT
SA3516252760cardiac blood WT
SA3516262717cardiac blood WT
SA3516272795-3fetus blood HET-het
SA3516282714-3fetus blood HET-het
SA3516292714-4fetus blood HET-het
SA3516302730-6fetus blood HET-het
SA3516312721-3fetus blood HET-het
SA3516322703-6fetus blood HET-het
SA3516332795-1fetus blood HET-het
SA3516342795-2fetus blood HET-het
SA3516352703-1fetus blood HET-het
SA3516362665-9fetus blood HET-het
SA3516372789-6fetus blood HET-het
SA3516382757-11fetus blood HET-het
SA3516392757-7fetus blood HET-het
SA3516402703-7fetus blood HET-het
SA3516412665-6fetus blood HET-het
SA3516422785-9fetus blood HET-het
SA3516432789-1fetus blood HET-het
SA3516442757-8fetus blood HET-het
SA3516452785-5fetus blood HET-het
SA3516462795-7fetus blood HET-het
SA3516472721-4fetus blood HET-hom
SA3516482748-1fetus blood HET-hom
SA3516492729-1fetus blood HET-hom
SA3516502740-1fetus blood HET-hom
SA3516512721-2fetus blood HET-hom
SA3516522748-2fetus blood HET-hom
SA3516532740-3fetus blood HET-hom
SA3516542716-1fetus blood HET-hom
SA3516552740-2fetus blood HET-hom
SA3516562775-5fetus blood HET-hom
SA3516572729-5fetus blood HET-hom
SA3516582775-2fetus blood HET-hom
SA3516592775-3fetus blood HET-hom
SA3516602729-4fetus blood HET-hom
SA3516612775-4fetus blood HET-hom
SA3516622729-6fetus blood HET-hom
SA3516632729-3fetus blood HET-hom
SA3516642763-1fetus blood HET-hom
SA3516652775-1fetus blood HET-hom
SA3516662738-5fetus blood WT-wt
SA3516672684-7fetus blood WT-wt
SA3516682684-1fetus blood WT-wt
SA3516692738-7fetus blood WT-wt
SA3516702738-1fetus blood WT-wt
SA3516712738-6fetus blood WT-wt
SA3516722684-4fetus blood WT-wt
SA3516732684-5fetus blood WT-wt
SA3516742732-9fetus blood WT-wt
SA3516752760-5fetus blood WT-wt
SA3516762760-2fetus blood WT-wt
SA3516772684-9fetus blood WT-wt
SA3516782738-3fetus blood WT-wt
SA3516792684-2fetus blood WT-wt
SA3516802760-6fetus blood WT-wt
SA3516812732-3fetus blood WT-wt
SA3516822732-6fetus blood WT-wt
SA3516832732-7fetus blood WT-wt
SA3516842760-4fetus blood WT-wt
SA3516852760-3fetus blood WT-wt
SA3516862684-3fetus blood WT-wt
SA3516872732-5fetus blood WT-wt
SA3516882684-8fetus blood WT-wt
SA3516892760-1fetus blood WT-wt
SA3516902730-2fetus blood WT-wt
Showing results 1 to 85 of 85
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