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RhoA in postnatal spinal motoneuron is essential for peripheral myelination

GSE339005 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2026/07/30 Platform GPL34290
Summary
Peripheral myelination requires precise axon-glia communication, yet the neuronal intrinsic machinery that governs the release of axonal signals remains incompletely understood. Here, we discover that RhoA, a classic cytoskeletal regulator, is highly expressed in postnatal spinal motoneurons and unexpectedly governs this axon-glia communication. RhoA conditional knockout in postnatal motoneurons causes profound peripheral hypomyelination without affecting neuronal survival, dendrites, or axonal caliber. Mechanistically, RhoA deficiency in postnatal spinal motoneurons attenuates ROCK2/p-Erk/SP1/BACE1 signaling and NRG1-III secretion, then disrupts Schwann cell’s differentiation, lipid biosynthesis, and myelin formation. Together, this study reveals a novel, non-cell-autonomous role for RhoA, and provides new insights into the complexity of neuronal control over peripheral myelination.
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Also filed as BioProject PRJNA1496770 and SRA study SRP718865. Searching any of these in the dataset finder brings you back here.

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