O-GlcNAc is required for the survival of primed pluripotent stem cells and their reversion to the naïve state

Miura, Taichi; Nishihara, Shoko

doi:10.1016/j.bbrc.2016.10.111

Cited by 16 publications

(20 citation statements)

References 23 publications

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“…Additionally, as previously mentioned, HBP couples macromolecular metabolism to O-GlcNAc modifications in proteins, including epigenetic modifiers (Figure 3) (94). Cycling of these posttranslational modifications by OGT and OGA are required for naïve and primed state induction, maintenance, and differentiation (95,96). OGT interacts with TET1 enzymes preferentially at transcription start sites, thereby influencing gene expression (58).…”

Section: Metabolism and The Naïve Psc Epigenomementioning

confidence: 99%

Metabolism in pluripotency: Both driver and passenger?

Dahan

Nguyen

et al. 2019

Journal of Biological Chemistry

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Downloaded from2 Pluripotent stem cells (PSCs) are highly proliferative cells characterized by robust metabolic demands to power rapid division. For many years considered a passive component or "passenger" of cell fate determination, cell metabolism is now starting to take center stage as a driver of cell fate outcomes. This review provides an update and analysis of our current understanding of PSC metabolism and its role in self-renewal, differentiation, and somatic cell reprogramming to pluripotency. Moreover, we present evidence on the active roles metabolism plays in shaping the epigenome to influence patterns of gene expression that may model key features of early embryonic development.Most investigators view metabolism, which encompasses the synthesis and utilization of macromolecules and energy, as a passive supporter of self-renewal and rapid proliferation in pluripotent stem cells (PSCs) 1 and their differentiated, slower dividing progeny. However, exciting recent studies are changing this perception by showing an active role for metabolism in PSC fate determination.

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Section: Metabolism and The Naïve Psc Epigenomementioning

confidence: 99%

Metabolism in pluripotency: Both driver and passenger?

Dahan

Nguyen

et al. 2019

Journal of Biological Chemistry

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“…As mentioned above, primed epiblast stem cells or epiblast stem cell‐like cells can be reverted to naïve ES cell‐like cells by culturing in medium containing LIF, Wnt accelerator, and Mek inhibitor . Both LacdiNAc expression and LIF/Stat3 signaling contribute to reversion from primed to naïve state (Fig.…”

Section: Roles Of Glycans In Mammalian Pluripotent Stem Cellsmentioning

confidence: 86%

“…Naïve mouse ES cells can be differentiated to primed epiblast stem cell‐like cells by culturing and passaging in medium containing FGF2 and Activin A or FGF2 and JAK inhibitor 1 (LIF inhibitor) , instead of LIF. Conversely, primed epiblast stem cells or epiblast stem cell‐like cells can be reverted to naïve ES cell‐like cells by culturing and passaging in medium containing LIF, Wnt accelerator (CHIR99021, CHIR), and Mek inhibitor (PD0325901, PD03), instead of FGF . However, prolonged culture under these conditions should be avoided because prolonged culture with Mek inhibitor results in irreversible epigenetic changes that impair developmental potential .…”

Section: Roles Of Glycans In Mammalian Pluripotent Stem Cellsmentioning

confidence: 99%

“…Naïve mouse ES cells can be converted to primed epiblast stem cell‐like cells by culturing and passaging in medium containing FGF2 and Activin A or FGF2 and JAK inhibitor 1 , instead of LIF. During the transition from naïve to primed state, HS 3‐ O ‐sulfotransferase 5 (HS3OST‐5) and its product, 3‐ O ‐sulfated HS, increase (Fig.…”

Section: Roles Of Glycans In Mammalian Pluripotent Stem Cellsmentioning

confidence: 99%

“…Recently, glycan function in the primed state has begun to be clarified using primed pluripotent stem cells. Ogt is required for survival of primed mouse pluripotent stem cells, namely primed epiblast stem cell‐like cells derived from naïve mouse ES cells . However, OGT is not involved in maintaining the undifferentiated primed state.…”

Section: Roles Of Glycans In Mammalian Pluripotent Stem Cellsmentioning

confidence: 99%

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Glycans in stem cell regulation: from Drosophila tissue stem cells to mammalian pluripotent stem cells

Nishihara

2018

FEBS Letters

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Cell surface glycans, which are tissue-specific and developmentally regulated, work as essential modulators in ligand-receptor interactions, binding to various signal ligands including Wnt, Hedgehog, fibroblast growth factors, epidermal growth factors, and bone morphogenetic proteins, as well as in cell-cell interactions and cell-extracellular matrix interactions. These signals are essential for the stemness and differentiation of various kinds of stem cells. In addition, the intracellular O-linked N-acetylglucosamine, a form of glycosylation found only on nuclear or cytoplasmic proteins, regulates core transcription factors of stemness and phosphorylation of downstream signal components. Therefore, various kinds of glycans regulate the stem cell status; the structures of many of which are evolutionarily conserved from Drosophila to mammals. Understanding the molecular mechanisms of glycans in stemness and differentiation is increasingly important for innovative clinical applications, as well as for basic research. This Review focuses on the roles of glycans in Drosophila tissue stem cells and mammalian pluripotent stem cells.

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Regulation of 3-O-Sulfation of Heparan Sulfate During Transition from the Naïve to the Primed State in Mouse Embryonic Stem Cells

Ota

Nishihara

2021

Methods in Molecular Biology

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O-GlcNAc is required for the survival of primed pluripotent stem cells and their reversion to the naïve state

Cited by 16 publications

References 23 publications

Metabolism in pluripotency: Both driver and passenger?

Metabolism in pluripotency: Both driver and passenger?

Glycans in stem cell regulation: from Drosophila tissue stem cells to mammalian pluripotent stem cells

Regulation of 3-O-Sulfation of Heparan Sulfate During Transition from the Naïve to the Primed State in Mouse Embryonic Stem Cells

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