The membrane palmitoylated protein, MPP6, is involved in myelin formation in the mouse peripheral nervous system

Yurika Saitoh1,2, Akio Kamijo1, Junji Yamauchi3

  • 1Health Science Division, Department of Medical Sciences, Graduate School of Medicine, Science and Technology, Shinshu University, 3-1-1 Asahi, Matsumoto City, Nagano, 390-8621, Japan.

Insights

The MPP6-Lin7 protein complex is crucial for regulating myelin formation in the peripheral nervous system. Its absence in mice leads to thicker myelin, indicating a key role in myelin structure.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Schwann cells in the peripheral nervous system (PNS) contain a membrane skeletal complex involving protein 4.1G, membrane palmitoylated protein 6 (MPP6), Lin7, and cell adhesion molecule 4 (CADM4).
  • This complex, particularly MPP6, Lin7, and CADM4, is transported to Schmidt-Lanterman incisures (SLIs) by protein 4.1G.

Purpose of the Study:

  • To investigate the role of MPP6 in myelin structure and protein complex formation within the PNS.
  • To elucidate the function of the MPP6-Lin7 complex in Schwann cells and myelin maintenance.

Main Methods:

  • Generation and analysis of MPP6-deficient mice.
  • Immunohistochemistry and western blotting to assess protein localization and levels.
  • Electron microscopy to evaluate sciatic nerve myelin structure.
  • Tail-suspension test to assess motor activity.

Main Results:

  • In MPP6-deficient mice, Lin7 was significantly reduced in SLIs, while CADM4 and 4.1G localization and amounts remained unchanged.
  • No significant impairment in motor activity was observed in MPP6-deficient mice.
  • Electron microscopy revealed significantly thicker myelin in the internodes of sciatic nerves from MPP6-deficient mice compared to wild-type controls.

Conclusions:

  • The MPP6-Lin7 protein complex plays a regulatory role in myelin formation and structure within the PNS.
  • MPP6 deficiency alters myelin thickness, suggesting its involvement in myelin homeostasis.

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