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Transcriptomic changes in mouse Epiblast stem cells induced with Mixl1

ABSTRACT: We performed total RNA-seq in a epiblast stem cell model of mouse gastrulation to determine the effect of Mixl1 knockout and induction.

ORGANISM(S): Mus musculus

PROVIDER: GSE161165 | GEO | 2024/07/27

REPOSITORIES: GEO

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Chromatin accessibility in mouse Epiblast stem cells induced with Mixl1

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Chromatin accessibility in mouse Epiblast stem cells induced with Mixl1

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Project description:During mouse gastrulation, the formation of germ layers proceeds concurrently with the transition pluripotency state and the allocation of the multipotent epiblast cells to the germ layer derivatives. Lineage analysis and fate-mapping studies have revealed that groups of cells in different regions of the epiblast and the primitive streak of the gastrulating embryo are allocated to separate progenitors of the ectoderm, mesoderm and endoderm lineages three germ layers with descendants of each progenitor contributing to specific types of germ layer derivatives. Spatiotemporal transcriptomic analysis of the epiblast cell population has inferred that besides the allocation of the epiblast cells to progenitors of germ layers, a population of putative mesendoderm progenitors may be present in the gastrulating embryos.

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Project description:Identification of Ta and Tbx16 binding sites during gastrulation, and Mixl1 binding sites during endoderm specification

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hESC MIXL1+ MIXL1- microarray

Project description:Microarray analysis of isolated hES cells from day 3 of cardiac differentiation was used to identify differences between MIXL1eGFP+ and MIXL1eGFP- transcriptomes. We identified 6,757 differentially regulated genes, of which 2,520 were upregulated â¥2-fold in the eGFP+ (MIXL1+) mesoderm population A stencil differentiation protocol was used to isolate mesodermal cells based on GFP expression from the MIXL1 locus. Microarray analysis of isolated cells from day 3 of differentiation was used to identify differences between MIXL1eGFP+ and MIXL1eGFP- transcriptomes.

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The epigenetic modifier Fam208a is required to maintain epiblast cell potency

Project description:Gastrulation initiates with the formation of the primitive streak, during which, cells of the epiblast delaminate to form the mesoderm and definitive endoderm. At this stage, the pluripotent cell population of the epiblast undergoes very rapid cellular proliferation and extensive epigenetic programming. Here, we show that Fam208a, a new epigenetic modifier, is essential for early post-implantation development using mouse strains harbouring two different allelic mutations. We show that at E6.5, Fam208a mutants have a decreased number of Oct4-positive epiblast cells due to an increase in p53-driven apoptosis. Complete removal of p53 could rescue the gastrulation block in Fam208a mutants, enabling them to develop until E8.5-9.0. The data demonstrates a new in vivo function of Fam208a in maintaining epiblast fitness thereby, making it an important factor at the onset of gastrulation.

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