Abstract
Primordial germ cells (PGCs) and somatic cells originate from postimplantation epiblast cells in mice. As pluripotency is lost upon differentiation of somatic lineages, a naive epigenome and the pluripotency network are re-established during PGC development. Here we demonstrate that Prdm14 contributes not only to PGC specification, but also to naive pluripotency in embryonic stem (ES) cells by repressing the DNA methylation machinery and fibroblast growth factor (FGF) signalling. This indicates a critical role for Prdm14 in programming PGCs and promoting pluripotency in ES cells.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cell Differentiation
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DNA Methylation
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DNA-Binding Proteins
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Embryonic Stem Cells / cytology
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Embryonic Stem Cells / metabolism*
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Fibroblast Growth Factors / genetics*
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Fibroblast Growth Factors / metabolism
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Gene Expression Profiling
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Gene Expression Regulation, Developmental*
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Germ Cells / cytology
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Germ Cells / metabolism*
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Germ Layers / cytology
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Germ Layers / metabolism
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Mice
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Mice, Inbred C57BL
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Mice, Transgenic
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Mitogen-Activated Protein Kinases / genetics
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Mitogen-Activated Protein Kinases / metabolism
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Pluripotent Stem Cells / cytology
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Pluripotent Stem Cells / metabolism*
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RNA-Binding Proteins
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Signal Transduction
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Transcription Factors / genetics*
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Transcription Factors / metabolism
Substances
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DNA-Binding Proteins
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Prdm14 protein, mouse
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RNA-Binding Proteins
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Transcription Factors
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Fibroblast Growth Factors
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Mitogen-Activated Protein Kinases