{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE339nnn/GSE339005/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE339005"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"RhoA in postnatal spinal motoneuron is essential for peripheral myelination","description":"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.","dates":{"publication":"2026/07/30"},"accession":"GSE339005","cross_references":{"GSM":["GSM9886353","GSM9886352","GSM9886355","GSM9886354","GSM9886357","GSM9886356"],"GPL":["34290"],"GSE":["339005"],"taxon":["Mus musculus"]}}