PUBLICATION

TET1-mediated DNA hydroxymethylation regulates adult remyelination in mice

Authors
Moyon, S., Frawley, R., Marechal, D., Huang, D., Marshall-Phelps, K.L.H., Kegel, L., Bøstrand, S.M.K., Sadowski, B., Jiang, Y.H., Lyons, D.A., Möbius, W., Casaccia, P.
ID
ZDB-PUB-210609-4
Date
2021
Source
Nature communications   12: 3359 (Journal)
Registered Authors
Kegel, Linde, Lyons, David A.
Keywords
none
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Cells, Cultured
  • DNA Methylation*
  • DNA-Binding Proteins/genetics*
  • DNA-Binding Proteins/metabolism
  • Gene Expression Profiling/methods*
  • Mice, Knockout
  • Mice, Transgenic
  • Mutation
  • Myelin Sheath/genetics*
  • Myelin Sheath/metabolism
  • Oligodendroglia/cytology
  • Oligodendroglia/metabolism
  • Proto-Oncogene Proteins/genetics*
  • Proto-Oncogene Proteins/metabolism
  • RNA-Seq/methods
  • Remyelination/genetics*
  • Solute Carrier Family 12, Member 2/genetics
  • Solute Carrier Family 12, Member 2/metabolism
  • Zebrafish/genetics
PubMed
34099715 Full text @ Nat. Commun.
Abstract
The mechanisms regulating myelin repair in the adult central nervous system (CNS) are unclear. Here, we identify DNA hydroxymethylation, catalyzed by the Ten-Eleven-Translocation (TET) enzyme TET1, as necessary for myelin repair in young adults and defective in old mice. Constitutive and inducible oligodendrocyte lineage-specific ablation of Tet1 (but not of Tet2), recapitulate this age-related decline in repair of demyelinated lesions. DNA hydroxymethylation and transcriptomic analyses identify TET1-target in adult oligodendrocytes, as genes regulating neuro-glial communication, including the solute carrier (Slc) gene family. Among them, we show that the expression levels of the Na+/K+/Cl- transporter, SLC12A2, are higher in Tet1 overexpressing cells and lower in old or Tet1 knockout. Both aged mice and Tet1 mutants also present inefficient myelin repair and axo-myelinic swellings. Zebrafish mutants for slc12a2b also display swellings of CNS myelinated axons. Our findings suggest that TET1 is required for adult myelin repair and regulation of the axon-myelin interface.
Genes / Markers
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Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
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Antibodies
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Mapping