Loss of Bright/Arid3A reprograms MEFs to a pluripotent state
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE52692 | GEO | 2013/11/25
SECONDARY ACCESSION(S): PRJNA229818
REPOSITORIES: GEO
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Project description:Bright null mouse embryonic stem cells and spontaneously reprogrammed Bright null cells compared to WT mouse embryonic stem cells;Work further described in Popowski et. al 2013 Bright null mouse embryonic stem cells and wildtype mouse embryonic stem cells differentiated in embryoid bodies at day 6 and day 15 Total RNA from each cell line using indicated replicates
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Project description:Previous studies in the mouse indicated that Arid3a plays a critical role in the first cell fate decision required for generation of trophectoderm (TE). Here, we demonstrate that Arid3a is widely expressed during mouse and human placentation and essential for early embryonic viability. Arid3a is located within trophoblast giant cells and other trophoblast-derived cell subtypes in the junctional and labyrinth zones of the placenta. Conventional Arid3a knockout embryos suffer restricted intrauterine growth with sever defects in placental structural organization. Arid3a null placentas show aberrant expression of subtype-specific markers as well as significant alteration in inflammatory response-related genes, cytokines and chemokines. We provide evidence that BMP4-mediated induction of trophoblast stem (TS)-like cells from human induced pluripotent (iPS) stem cells results in ARID3A upregulation and cytoplasmic to nuclear translocation. Overexpression of ARID3A in human iPS and BMP4-mediated TS-like cells up-regulated TE markers, whereas pluripotent markers were down-regulated. Our results indicate that the roles of Arid3a are conserved and essential for mammalian placental development through regulation of both intrinsic and extrinsic developmental programs. Placentas of E10.5 and E11.5 wild type (WT) and Arid3a-/- mice were generated by deep sequencing, using Illumina
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