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Nuclear Receptors in Regulation of Mouse ES Cell Pluripotency and Differentiation.

Mullen EM, Gu P, Cooney AJ - PPAR Res (2007)

Bottom Line: Embryonic stem (ES) cells have great therapeutic potential because they are capable of indefinite self-renewal and have the potential to differentiate into over 200 different cell types that compose the human body.The switch from the pluripotent phenotype to a differentiated cell involves many complex signaling pathways including those involving LIF/Stat3 and the transcription factors Sox2, Nanog and Oct-4.Here we review the roles of the nuclear receptors involved in regulating these important processes in ES cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.

ABSTRACT
Embryonic stem (ES) cells have great therapeutic potential because they are capable of indefinite self-renewal and have the potential to differentiate into over 200 different cell types that compose the human body. The switch from the pluripotent phenotype to a differentiated cell involves many complex signaling pathways including those involving LIF/Stat3 and the transcription factors Sox2, Nanog and Oct-4. Many nuclear receptors play an important role in the maintenance of pluripotence (ERRbeta, SF-1, LRH-1, DAX-1) repression of the ES cell phenotype (RAR, RXR, GCNF) and also the differentiation of ES cells (PPARgamma). Here we review the roles of the nuclear receptors involved in regulating these important processes in ES cells.

No MeSH data available.


Yin-yang regulation of Oct-4 expression during ES cell differentiation by LRH-1 and GCNF, which compete for the same element. In undifferentiated ES cells LRH-1 binds toelements in the Oct-4 proximal enhancer and proximal promoter to maintain itsexpression during the very earliest stages of differentiation. As differentiation progresses LRH-1 expression decreases and GCNF expression is induced. At an intermediate point GCNF displaces LRH-1 and represses Oct-4 by recruiting the DNA methylation machinery that ultimatelyleads to the silencing of Oct-4 expression in somatic cells.
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fig1: Yin-yang regulation of Oct-4 expression during ES cell differentiation by LRH-1 and GCNF, which compete for the same element. In undifferentiated ES cells LRH-1 binds toelements in the Oct-4 proximal enhancer and proximal promoter to maintain itsexpression during the very earliest stages of differentiation. As differentiation progresses LRH-1 expression decreases and GCNF expression is induced. At an intermediate point GCNF displaces LRH-1 and represses Oct-4 by recruiting the DNA methylation machinery that ultimatelyleads to the silencing of Oct-4 expression in somatic cells.

Mentions: Thus, GCNF is essential for the repression of pluripotency genes such as Oct-4 and Nanog, and also in the initiation of differentiation where both transcriptional and epigenetic mechanisms play a role in its function (see Figure 1).


Nuclear Receptors in Regulation of Mouse ES Cell Pluripotency and Differentiation.

Mullen EM, Gu P, Cooney AJ - PPAR Res (2007)

Yin-yang regulation of Oct-4 expression during ES cell differentiation by LRH-1 and GCNF, which compete for the same element. In undifferentiated ES cells LRH-1 binds toelements in the Oct-4 proximal enhancer and proximal promoter to maintain itsexpression during the very earliest stages of differentiation. As differentiation progresses LRH-1 expression decreases and GCNF expression is induced. At an intermediate point GCNF displaces LRH-1 and represses Oct-4 by recruiting the DNA methylation machinery that ultimatelyleads to the silencing of Oct-4 expression in somatic cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2233893&req=5

fig1: Yin-yang regulation of Oct-4 expression during ES cell differentiation by LRH-1 and GCNF, which compete for the same element. In undifferentiated ES cells LRH-1 binds toelements in the Oct-4 proximal enhancer and proximal promoter to maintain itsexpression during the very earliest stages of differentiation. As differentiation progresses LRH-1 expression decreases and GCNF expression is induced. At an intermediate point GCNF displaces LRH-1 and represses Oct-4 by recruiting the DNA methylation machinery that ultimatelyleads to the silencing of Oct-4 expression in somatic cells.
Mentions: Thus, GCNF is essential for the repression of pluripotency genes such as Oct-4 and Nanog, and also in the initiation of differentiation where both transcriptional and epigenetic mechanisms play a role in its function (see Figure 1).

Bottom Line: Embryonic stem (ES) cells have great therapeutic potential because they are capable of indefinite self-renewal and have the potential to differentiate into over 200 different cell types that compose the human body.The switch from the pluripotent phenotype to a differentiated cell involves many complex signaling pathways including those involving LIF/Stat3 and the transcription factors Sox2, Nanog and Oct-4.Here we review the roles of the nuclear receptors involved in regulating these important processes in ES cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.

ABSTRACT
Embryonic stem (ES) cells have great therapeutic potential because they are capable of indefinite self-renewal and have the potential to differentiate into over 200 different cell types that compose the human body. The switch from the pluripotent phenotype to a differentiated cell involves many complex signaling pathways including those involving LIF/Stat3 and the transcription factors Sox2, Nanog and Oct-4. Many nuclear receptors play an important role in the maintenance of pluripotence (ERRbeta, SF-1, LRH-1, DAX-1) repression of the ES cell phenotype (RAR, RXR, GCNF) and also the differentiation of ES cells (PPARgamma). Here we review the roles of the nuclear receptors involved in regulating these important processes in ES cells.

No MeSH data available.