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Keywords {🔍}

cells, nsun, mitochondrial, pubmed, escs, cell, article, differentiation, google, scholar, wildtype, fig, cas, stem, rna, levels, catcat, nsunmutant, ros, central, translation, expression, methylation, human, wnt, function, mttrnamet, embryonic, esc, protein, shown, proliferation, reduced, mouse, alkbh, performed, cytosine, mutant, pluripotency, medium, test, potential, trna, modification, increased, methyltransferase, modifications, found, mitochondria, glycolysis,

Topics {✒️}

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Questions {❓}

• Sherwood V (2015) WNT signaling: an emerging mediator of cancer cell metabolism?

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         headline:RNA cytosine methyltransferase Nsun3 regulates embryonic stem cell differentiation by promoting mitochondrial activity
         description:Chemical modifications of RNA have been attracting increasing interest because of their impact on RNA fate and function. Therefore, the characterization of enzymes catalyzing such modifications is of great importance. The RNA cytosine methyltransferase NSUN3 was recently shown to generate 5-methylcytosine in the anticodon loop of mitochondrial tRNAMet. Further oxidation of this position is required for normal mitochondrial translation and function in human somatic cells. Because embryonic stem cells (ESCs) are less dependent on oxidative phosphorylation than somatic cells, we examined the effects of catalytic inactivation of Nsun3 on self-renewal and differentiation potential of murine ESCs. We demonstrate that Nsun3-mutant cells show strongly reduced mt-tRNAMet methylation and formylation as well as reduced mitochondrial translation and respiration. Despite the lower dependence of ESCs on mitochondrial activity, proliferation of mutant cells was reduced, while pluripotency marker gene expression was not affected. By contrast, ESC differentiation was skewed towards the meso- and endoderm lineages at the expense of neuroectoderm. Wnt3 was overexpressed in early differentiating mutant embryoid bodies and in ESCs, suggesting that impaired mitochondrial function disturbs normal differentiation programs by interfering with cellular signalling pathways. Interestingly, basal levels of reactive oxygen species (ROS) were not altered in ESCs, but Nsun3 inactivation attenuated induction of mitochondrial ROS upon stress, which may affect gene expression programs upon differentiation. Our findings not only characterize Nsun3 as an important regulator of stem cell fate but also provide a model system to study the still incompletely understood interplay of mitochondrial function with stem cell pluripotency and differentiation.
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      headline:RNA cytosine methyltransferase Nsun3 regulates embryonic stem cell differentiation by promoting mitochondrial activity
      description:Chemical modifications of RNA have been attracting increasing interest because of their impact on RNA fate and function. Therefore, the characterization of enzymes catalyzing such modifications is of great importance. The RNA cytosine methyltransferase NSUN3 was recently shown to generate 5-methylcytosine in the anticodon loop of mitochondrial tRNAMet. Further oxidation of this position is required for normal mitochondrial translation and function in human somatic cells. Because embryonic stem cells (ESCs) are less dependent on oxidative phosphorylation than somatic cells, we examined the effects of catalytic inactivation of Nsun3 on self-renewal and differentiation potential of murine ESCs. We demonstrate that Nsun3-mutant cells show strongly reduced mt-tRNAMet methylation and formylation as well as reduced mitochondrial translation and respiration. Despite the lower dependence of ESCs on mitochondrial activity, proliferation of mutant cells was reduced, while pluripotency marker gene expression was not affected. By contrast, ESC differentiation was skewed towards the meso- and endoderm lineages at the expense of neuroectoderm. Wnt3 was overexpressed in early differentiating mutant embryoid bodies and in ESCs, suggesting that impaired mitochondrial function disturbs normal differentiation programs by interfering with cellular signalling pathways. Interestingly, basal levels of reactive oxygen species (ROS) were not altered in ESCs, but Nsun3 inactivation attenuated induction of mitochondrial ROS upon stress, which may affect gene expression programs upon differentiation. Our findings not only characterize Nsun3 as an important regulator of stem cell fate but also provide a model system to study the still incompletely understood interplay of mitochondrial function with stem cell pluripotency and differentiation.
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         5-Methylcytosine
         Mitochondria
         Bisulfite sequencing
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         Self-renewal
         Epitranscriptome
         Cell Biology
         Biomedicine
         general
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         Biochemistry
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               type:PostalAddress
            type:Organization
      name:Jakob Troppmair
      affiliation:
            name:Medical University of Innsbruck
            address:
               name:Daniel Swarovski Research Laboratory, Department of Visceral, Transplant, and Thoracic Surgery, Medical University of Innsbruck, Innsbruck, Austria
               type:PostalAddress
            type:Organization
      name:Alexandra Lusser
      url:http://orcid.org/0000-0002-2226-9081
      affiliation:
            name:Medical University of Innsbruck
            address:
               name:Division of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Division of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria
      name:Division of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria
      name:Division of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria
      name:Division of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria
      name:Daniel Swarovski Research Laboratory, Department of Visceral, Transplant, and Thoracic Surgery, Medical University of Innsbruck, Innsbruck, Austria
      name:Division of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria
      name:Division of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria
      name:Division of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria
      name:Division of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria
      name:Division of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria
      name:Zymo Research Corp., Irvine, USA
      name:Institute for Neuroscience, Medical University of Innsbruck, Innsbruck, Austria
      name:Daniel Swarovski Research Laboratory, Department of Visceral, Transplant, and Thoracic Surgery, Medical University of Innsbruck, Innsbruck, Austria
      name:Division of Molecular Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria

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