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Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE155046 | GEO | 2020/08/11

REPOSITORIES: GEO

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Premature Activation of Immune Transcription Programs in Autoimmune-Predisposed Mouse Embryonic Stem Cells and Blastocysts.

Project description:Autoimmune diabetes is a complex multifactorial disease with genetic and environmental factors playing pivotal roles. While many genes associated with the risk of diabetes have been identified to date, the mechanisms by which external triggers contribute to the genetic predisposition remain unclear. Here, we derived embryonic stem (ES) cell lines from diabetes-prone non-obese diabetic (NOD) and healthy C57BL/6 (B6) mice. While overall pluripotency markers were indistinguishable between newly derived NOD and B6 ES cells, we discovered several differentially expressed genes that normally are not expressed in ES cells. Several genes that reside in previously identified insulin-dependent diabetics (Idd) genomic regions were up-regulated in NOD ES cells. Gene set enrichment analysis showed that different groups of genes associated with immune functions are differentially expressed in NOD. Transcriptomic analysis of NOD blastocysts validated several differentially overexpressed Idd genes compared to B6. Genome-wide mapping of active histone modifications using ChIP-Seq supports active expression as the promoters and enhancers of activated genes are also marked by active histone modifications. We have also found that NOD ES cells secrete more inflammatory cytokines. Our data suggest that the known genetic predisposition of NOD to autoimmune diabetes leads to epigenetic instability of several Idd regions.

| S-EPMC7460978 | biostudies-literature

Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

Project description:To study the underlying mechanism of autoimmunity predisposition in autoimmune-prone mouse strains, we characterize embryonic stem cells derived from various mouse strains.

2020-08-11 | GSE155045 | GEO

Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

Project description:To study the underlying mechanism of autoimmunity predisposition in autoimmune-proned mouse strains, we characterize embryonic stem cells derived from various mouse strains.

2020-08-11 | GSE155044 | GEO

Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

Project description:To study the underlying mechanism of autoimmunity predisposition in autoimmune-prone mouse strains, we characterize embryonic stem cells derived from various mouse strains.

2020-08-11 | GSE154458 | GEO

Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

Project description:Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

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Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

Project description:Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

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Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

Project description:Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

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Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

Project description:Premature activation of immune transcription programs in autoimmune-predisposed mouse embryonic stem cells and blastocysts

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Germline competent embryonic stem cells derived from rat blastocysts.

Project description:Rats have important advantages over mice as an experimental system for physiological and pharmacological investigations. The lack of rat embryonic stem (ES) cells has restricted the availability of transgenic technologies to create genetic models in this species. Here, we show that rat ES cells can be efficiently derived, propagated, and genetically manipulated in the presence of small molecules that specifically inhibit GSK3, MEK, and FGF receptor tyrosine kinases. These rat ES cells express pluripotency markers and retain the capacity to differentiate into derivatives of all three germ layers. Most importantly, they can produce high rates of chimerism when reintroduced into early stage embryos and can transmit through the germline. Establishment of authentic rat ES cells will make possible sophisticated genetic manipulation to create models for the study of human diseases.

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A Myc network accounts for similarities between embryonic stem and cancer cell transcription programs.

Project description:c-Myc (Myc) is an important transcriptional regulator in embryonic stem (ES) cells, somatic cell reprogramming, and cancer. Here, we identify a Myc-centered regulatory network in ES cells by combining protein-protein and protein-DNA interaction studies and show that Myc interacts with the NuA4 complex, a regulator of ES cell identity. In combination with regulatory network information, we define three ES cell modules (Core, Polycomb, and Myc) and show that the modules are functionally separable, illustrating that the overall ES cell transcription program is composed of distinct units. With these modules as an analytical tool, we have reassessed the hypothesis linking an ES cell signature with cancer or cancer stem cells. We find that the Myc module, independent of the Core module, is active in various cancers and predicts cancer outcome. The apparent similarity of cancer and ES cell signatures reflects, in large part, the pervasive nature of Myc regulatory networks.

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