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Progressive axonopathy when oligodendrocytes lack the myelin protein CMTM5

Tobias J Buscham1, Maria A Eichel-Vogel1, Anna M Steyer1,2

  • 1Department of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.

Elife
|March 11, 2022
PubMed

Insights

Chemokine-like factor-like MARVEL-transmembrane domain containing protein 5 (CMTM5) is crucial for oligodendrocyte function in maintaining axon integrity. Its absence leads to progressive axonopathy, suggesting a role beyond myelin development.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Oligodendrocytes are vital for axonal health and rapid nerve impulse transmission.
  • The specific functions of many myelin proteins, including CMTM5, remain unclear.
  • CMTM5 is a tetraspan transmembrane protein highly expressed in the central nervous system (CNS) and myelin.

Purpose of the Study:

  • To investigate the functional role of CMTM5 in oligodendrocytes and CNS myelin.
  • To determine if CMTM5 is essential for myelin development, structure, or axonal maintenance.

Main Methods:

  • Genetic disruption of the Cmtm5 gene in oligodendrocytes of mice.
  • Analysis of CNS myelin development and ultrastructure.
  • Assessment of axonopathy in global and inducible Cmtm5 mutant mice.
  • Evaluation of the effect of the Wld mutation on the observed axonopathy.

Main Results:

  • Oligodendroglial Cmtm5 deficiency did not affect CNS myelin development or ultrastructure.
  • Absence of CMTM5 in oligodendrocytes led to early-onset, progressive axonopathy.
  • The Wld mutation partially ameliorated the axonopathy, indicating a Wallerian degeneration-like process.
  • CMTM5 deficiency in oligodendrocytes causes axon degeneration.

Conclusions:

  • CMTM5 plays a critical role in maintaining axonal integrity, independent of myelin biogenesis.
  • Oligodendrocyte-specific CMTM5 is essential for long-term axonal health.
  • The findings suggest CMTM5 is a key player in preventing neurodegenerative processes in the CNS.
Keywords:
axon degenerationaxon/glia-interactiondifferential myelin proteome analysisfocused ion beam scanning electron microscopymousemyelin sheathneuroscienceoligodendrocyte

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