Oligodendrocyte calcium signaling promotes actin-dependent myelin sheath extension

Manasi Iyer, Husniye Kantarci, Madeline H. Cooper, Nicholas Ambiel, Sammy Weiser Novak, Leonardo R. Andrade, Mable Lam, Graham Jones, Alexandra E. Münch, Xinzhu Yu, Baljit S. Khakh, Uri Manor and J. Bradley Zuchero ()
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Manasi Iyer: Stanford University School of Medicine
Husniye Kantarci: Stanford University School of Medicine
Madeline H. Cooper: Stanford University School of Medicine
Nicholas Ambiel: Stanford University School of Medicine
Sammy Weiser Novak: Salk Institute for Biological Studies
Leonardo R. Andrade: Salk Institute for Biological Studies
Mable Lam: Stanford University School of Medicine
Graham Jones: Stanford University School of Medicine
Alexandra E. Münch: Stanford University School of Medicine
Xinzhu Yu: University of Illinois at Urbana-
Baljit S. Khakh: University of California, Los Angeles
Uri Manor: Salk Institute for Biological Studies
J. Bradley Zuchero: Stanford University School of Medicine

Nature Communications, 2024, vol. 15, issue 1, 1-20

Abstract: Abstract Myelin is essential for rapid nerve signaling and is increasingly found to play important roles in learning and in diverse diseases of the CNS. Morphological parameters of myelin such as sheath length are thought to precisely tune conduction velocity, but the mechanisms controlling sheath morphology are poorly understood. Local calcium signaling has been observed in nascent myelin sheaths and can be modulated by neuronal activity. However, the role of calcium signaling in sheath formation remains incompletely understood. Here, we use genetic tools to attenuate oligodendrocyte calcium signaling during myelination in the developing mouse CNS. Surprisingly, genetic calcium attenuation does not grossly affect the number of myelinated axons or myelin thickness. Instead, calcium attenuation causes myelination defects resulting in shorter, dysmorphic sheaths. Mechanistically, calcium attenuation reduces actin filaments in oligodendrocytes, and an intact actin cytoskeleton is necessary and sufficient to achieve accurate myelin morphology. Together, our work reveals a cellular mechanism required for accurate CNS myelin formation and may provide mechanistic insight into how oligodendrocytes respond to neuronal activity to sculpt and refine myelin sheaths.

Date: 2024
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DOI: 10.1038/s41467-023-44238-3

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