Description
Formation of myelin by Schwann cells is tightly coupled to peripheral nervous system development and is important for neuronal function and long-term maintenance. Perturbation of myelin causes a number of specific disorders that are among the most prevalent diseases affecting the nervous system. Schwann cells synthesize myelin lipids de novo rather than relying on uptake of circulating lipids, yet one unresolved matter is how Acetyl CoA, a central metabolite in lipid formation is generated during myelin formation and maintenance. Recent studies have shown that glucose-derived Acetyl CoA itself is not required for myelination. Moreover, the importance of mitochondrially-derived Acetyl CoA has never been tested for myelination in vivo. Therefore, we have developed a Schwann cell-specific knockout of the ATP Citrate Lyase (Acly) gene to determine the importance of mitochondrial metabolism to supply Acetyl CoA in nerve development. Intriguingly, the ACLY pathway is important for myelin maintenance rather than myelin formation. In addition, ACLY is required to maintain expression of a myelin-associated gene program and to inhibit activation of the latent Schwann cell injury program.
[doi:10.25345/C5BC3T79Z]
[dataset license: CC0 1.0 Universal (CC0 1.0)]
Keywords: ACLY knockout, sciatic nerve, histone PTM
Contact
Principal Investigators:
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John Denu, University of Wisconsin - Madison, United States
John Svaren, University of Wisconsin-Madison, United States
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earmstrong
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GNPS content goes here (MSV000094403 [task=e923c22bd42340eda5a446110f033386])
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