ERG-associated protein with SET domain (ESET)-Oct4 interaction regulates pluripotency and represses the trophectoderm lineage

Yeap, Leng-Siew; Hayashi, Kozaburo; Surani, M. Azim

doi:10.1186/1756-8935-2-12

Cited by 112 publications

(111 citation statements)

References 36 publications

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“…5g-j). Furthermore, ES cells transfected with the ESET siRNA exhibited a classic differentiated morphology, which is consistent with previous observations 43,44 (Fig. 5k).…”

Section: Applying Pafcs To Quantify Tf Diffusion In Living Embryossupporting

confidence: 92%

“…S11). The ESET siRNA and SIM mutation also led to smaller dwell times of the free fraction of Oct4-paGFP, which suggests that part of the free fraction might interact with ESET independently of DNA binding in line with previous work 43 . Thus, our results in embryos and ES cells show that Oct4-paGFP diffusion properties depend not only on DNA interactions, but also on the TF's ability to interact with ESET.…”

Section: Applying Pafcs To Quantify Tf Diffusion In Living Embryossupporting

confidence: 88%

“…The methyltransferase ERG-associated protein with SET domain (ESET) was recently identified as a binding partner of Oct4 important for pluripotency 43,44 .…”

Section: Applying Pafcs To Quantify Tf Diffusion In Living Embryosmentioning

confidence: 99%

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Probing transcription factor diffusion dynamics in the living mammalian embryo with photoactivatable fluorescence correlation spectroscopy

et al. 2013

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Transcription factors use diffusion to search the DNA, yet the mechanisms controlling transcription factor diffusion during mammalian development remain poorly understood. Here we combine photoactivation and fluorescence correlation spectroscopy to study transcription factor diffusion in developing mouse embryos. We show that the pluripotencyassociated transcription factor Oct4 displays both fast and Brownian and slower subdiffusive behaviours that are controlled by DNA interactions. Following cell lineage specification, the slower DNA-interacting diffusion fraction distinguishes pluripotent from extraembryonic cell nuclei. Similar to Oct4, Sox2 shows slower diffusion in pluripotent cells while Cdx2 displays opposite dynamics, suggesting that slow diffusion may represent a general feature of transcription factors in lineages where they are essential. Slow Oct4 subdiffusive behaviours are conserved in embryonic stem cells and induced pluripotent stem cells (iPS cells), and lost during differentiation. We also show that Oct4 diffusion depends on its interaction with ERGassociated protein with SET domain. Photoactivation and fluorescence correlation spectroscopy provides a new intravital approach to study transcription factor diffusion in complex in vivo systems.

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“…5g-j). Furthermore, ES cells transfected with the ESET siRNA exhibited a classic differentiated morphology, which is consistent with previous observations 43,44 (Fig. 5k).…”

Section: Applying Pafcs To Quantify Tf Diffusion In Living Embryossupporting

confidence: 92%

Section: Applying Pafcs To Quantify Tf Diffusion In Living Embryossupporting

confidence: 88%

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Probing transcription factor diffusion dynamics in the living mammalian embryo with photoactivatable fluorescence correlation spectroscopy

et al. 2013

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“…While this manuscript was in revision, similar results were described by three other groups using RNAi mediated knock-down strategies of KMT1E in ES cells [47][48][49], thus confirming KMT1E's role in epigenetic control of euchromatic gene regulation and maintenance of the pluripotent state in ES cells.…”

Section: Discussionsupporting

confidence: 80%

KMT1E Mediated H3K9 Methylation Is Required for the Maintenance of Embryonic Stem Cells by Repressing Trophectoderm Differentiation

Lohmann

Loureiro

et al. 2009

Stem Cells

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Dynamic regulation of histone methylation by methyltransferases and demethylases plays a central role in regulating the fate of embryonic stem (ES) cells. The histone H3K9 methyltransferase KMT1E, formerly known as ESET or Setdb1, is essential to embryonic development as the ablation of the Setdb1 gene results in peri-implantation lethality and prevents the propagation of ES cells. However, Setdb1-null blastocysts do not display global changes in H3K9 methylation or DNA methylation, arguing against a genome-wide defect. Here we show that conditional deletion of the Setdb1 gene in ES cells results in the upregulation of lineage differentiation markers, especially trophectoderm-specific factors, similar to effects observed upon loss of Oct3/4 expression in ES cells. We demonstrate that KMT1E deficiency in ES cells leads to a decrease in histone H3K9 methylation at and derepression of trophoblast-associated genes such as Cdx2. Furthermore, we find genes that are derepressed upon Setdb1 deletion to overlap with known targets of polycomb mediated repression, suggesting that KMT1E mediated H3K9 methylation acts in concert with polycomb controlled H3K27 methylation. Our studies thus demonstrate an essential role for KMT1E in the control of developmentally regulated gene expression programs in ES cells.

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“…ESCs lacking Kmt1e (also called Setdb1 or Eset), an H3K9-specific HMT, fail to self-renew while acquiring trophectoderm properties [75][76][77][78]. Consistent with its role in ESCs, depletion of Kmt1e reduces the reprogramming efficiency in iPSCs generation [74].…”

Section: H3k4 Methylationmentioning

confidence: 98%

Embryonic stem cell and induced pluripotent stem cell: an epigenetic perspective

2012

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ERG-associated protein with SET domain (ESET)-Oct4 interaction regulates pluripotency and represses the trophectoderm lineage

Cited by 112 publications

References 36 publications

Probing transcription factor diffusion dynamics in the living mammalian embryo with photoactivatable fluorescence correlation spectroscopy

Probing transcription factor diffusion dynamics in the living mammalian embryo with photoactivatable fluorescence correlation spectroscopy

KMT1E Mediated H3K9 Methylation Is Required for the Maintenance of Embryonic Stem Cells by Repressing Trophectoderm Differentiation

Embryonic stem cell and induced pluripotent stem cell: an epigenetic perspective

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