Nonvesicular lipid transfer drives myelin growth in the central nervous system

Jianping Wu, Georg Kislinger, Jerome Duschek, Ayşe Damla Durmaz, Benedikt Wefers, Ruoqing Feng, Karsten Nalbach, Wolfgang Wurst, Christian Behrends, Martina Schifferer and Mikael Simons ()
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Jianping Wu: Technical University of Munich
Georg Kislinger: Technical University of Munich
Jerome Duschek: Ludwig-Maximilians-University München
Ayşe Damla Durmaz: Technical University of Munich
Benedikt Wefers: German Center for Neurodegenerative Diseases
Ruoqing Feng: Technical University of Munich
Karsten Nalbach: Ludwig-Maximilians-University München
Wolfgang Wurst: German Center for Neurodegenerative Diseases
Christian Behrends: Ludwig-Maximilians-University München
Martina Schifferer: German Center for Neurodegenerative Diseases
Mikael Simons: Technical University of Munich

Nature Communications, 2024, vol. 15, issue 1, 1-15

Abstract: Abstract Oligodendrocytes extend numerous cellular processes that wrap multiple times around axons to generate lipid-rich myelin sheaths. Myelin biogenesis requires an enormously productive biosynthetic machinery for generating and delivering these large amounts of newly synthesized lipids. Yet, a complete understanding of this process remains elusive. Utilizing volume electron microscopy, we demonstrate that the oligodendroglial endoplasmic reticulum (ER) is enriched in developing myelin, extending into and making contact with the innermost myelin layer where growth occurs. We explore the possibility of transfer of lipids from the ER to myelin, and find that the glycolipid transfer protein (GLTP), implicated in nonvesicular lipid transport, is highly enriched in the growing myelin sheath. Mice with a specific knockout of Gltp in oligodendrocytes exhibit ER pathology, hypomyelination and a decrease in myelin glycolipid content. In summary, our results demonstrate a role for nonvesicular lipid transport in CNS myelin growth, revealing a cellular pathway in developmental myelination.

Date: 2024
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DOI: 10.1038/s41467-024-53511-y

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