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PCL2 modulates gene regulatory networks controlling self-renewal and commitment in embryonic stem cells Walker E; Manias JL; Chang WY; Stanford WLCell Cycle 2011[Jan]; 10 (1): 45-51Recent reports have better elucidated the components of the Polycomb Repressive Complex 2 (PRC2) and its functional role in embryonic stem cells (ESCs) and their differentiated derivatives. The depletion of a newly described mammalian PRC2 associated protein, PCL2, leads to an increase in ESC self-renewal and a delay in differentiation, a phenotype similar to knockouts of the core PRC2 members. Genomic and cell biology data suggest that PCL2 is important in cell fate decisions and may play a role in recruitment of PRC2 to target genes and histone methylation. Importantly, depletion of PCL2 in ESCs leads to a decrease in 3meH3K27 at the proximal promoter regions of pluripotency transcription factors Tbx3, Klf4, Foxd3 and a concomitant increase in gene expression. These proteins subsequently activate expression of Oct4, Nanog and Sox2 through a feed-forward gene regulatory circuit, altering the core pluripotency network and driving cell fate decisions towards self-renewal. We propose a model whereby alteration of the epigenetic state of Tbx3, Klf4, and Foxd3 results in the enforced expression of the pluripotency network, preventing differentiation.|Amino Acid Sequence[MESH]|Animals[MESH]|Cell Differentiation/physiology[MESH]|Cyclins/physiology[MESH]|Drosophila Proteins/*physiology[MESH]|Embryonic Stem Cells/cytology/*physiology[MESH]|Gene Regulatory Networks/*physiology[MESH]|Histone-Lysine N-Methyltransferase/*physiology[MESH]|Humans[MESH]|Kruppel-Like Factor 4[MESH]|Molecular Sequence Data[MESH]|Polycomb-Group Proteins[MESH]|Repressor Proteins/physiology[MESH]|Saccharomyces cerevisiae Proteins/physiology[MESH] |
