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Structure-function Studies in Mouse Embryonic Stem Cells Using Recombinase-mediated Cassette Exchange
Published on: April 27, 2017
Sequence-specific regulator Prdm14 safeguards mouse ESCs from entering extraembryonic endoderm fates
Ziyang Ma1, Tomek Swigut, Anton Valouev
1Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, California, USA.
Nature Structural & Molecular Biology
|December 25, 2010
Summary
Prdm14 protein maintains mouse embryonic stem cell (mESC) identity by blocking differentiation into extraembryonic endoderm (ExEn). It acts as both a repressor and activator, influencing key self-renewal and differentiation genes.
Area of Science:
- Developmental Biology
- Stem Cell Biology
- Epigenetics
Background:
- Prdm14 is a transcription factor expressed in pluripotent cells.
- Its precise role in maintaining embryonic stem cell (ESC) identity is not fully understood.
Purpose of the Study:
- To investigate the function of Prdm14 in mouse ESC (mESC) maintenance and differentiation.
- To elucidate the molecular mechanisms by which Prdm14 regulates cell fate decisions.
Main Methods:
- Analysis of Prdm14 expression in mESCs and early embryos.
- Functional studies involving Prdm14 knockdown and overexpression in mESCs.
- Chromatin immunoprecipitation sequencing (ChIP-seq) to identify Prdm14-bound genomic regions.
- Reporter assays to assess transcriptional regulation.
Main Results:
- Prdm14 expression is restricted to pluripotent cells.
- Prdm14 prevents the induction of extraembryonic endoderm (ExEn) fates in mESCs.
- Overexpression of Prdm14 inhibits ExEn differentiation.
- Prdm14 directly represses genes involved in ExEn differentiation and activates genes promoting mESC self-renewal.
- Prdm14 shares genomic binding sites with key pluripotency factors Nanog and Oct4.
Conclusions:
- Prdm14 is a crucial regulator of mESC identity, acting as a molecular switch.
- It safeguards pluripotency by actively repressing differentiation pathways and promoting self-renewal.
- Prdm14 integrates into the core transcriptional network governing stem cell fate.
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