{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T07:03:19Z","timestamp":1791270199527,"version":"4.1.0"},"reference-count":29,"publisher":"National Academy of Sciences","issue":"19","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2011,5,10]]},"abstract":"<jats:p>During peripheral nerve development, Schwann cells ensheathe axons and form myelin to enable rapid and efficient action potential propagation. Although myelination requires profound changes in Schwann cell shape, how neuron\u2013glia interactions converge on the Schwann cell cytoskeleton to induce these changes is unknown. Here, we demonstrate that the submembranous cytoskeletal proteins \u03b1II and \u03b2II spectrin are polarized in Schwann cells and colocalize with signaling molecules known to modulate myelination in vitro. Silencing expression of these spectrins inhibited myelination in vitro, and remyelination in vivo. Furthermore, myelination was disrupted in motor nerves of zebrafish lacking \u03b1II spectrin. Finally, we demonstrate that loss of spectrin significantly reduces both F-actin in the Schwann cell cytoskeleton and the Nectin-like protein, Necl4, at the contact site between Schwann cells and axons. Therefore, we propose \u03b1II and \u03b2II spectrin in Schwann cells integrate the neuron\u2013glia interactions mediated by membrane proteins into the actin-dependent cytoskeletal rearrangements necessary for myelination.<\/jats:p>","DOI":"10.1073\/pnas.1019600108","type":"journal-article","created":{"date-parts":[[2011,4,25]],"date-time":"2011-04-25T23:05:55Z","timestamp":1303772755000},"page":"8009-8014","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":56,"title":["Schwann cell spectrins modulate peripheral nerve myelination"],"prefix":"10.1073","volume":"108","author":[{"given":"Keiichiro","family":"Susuki","sequence":"first","affiliation":[{"name":"Department of Neuroscience, Baylor College of Medicine, Houston, TX 77030;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alya R.","family":"Raphael","sequence":"additional","affiliation":[{"name":"Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasuhiro","family":"Ogawa","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Baylor College of Medicine, Houston, TX 77030;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael C.","family":"Stankewich","sequence":"additional","affiliation":[{"name":"Department of Pathology, Yale University, New Haven, CT 06520; 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