{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,12]],"date-time":"2025-10-12T19:46:40Z","timestamp":1760298400741},"reference-count":55,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2012,2,7]],"date-time":"2012-02-07T00:00:00Z","timestamp":1328572800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Comparative Neurology"],"published-print":{"date-parts":[[2012,4,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Mutations in human <jats:italic>LIS1<\/jats:italic> cause abnormal neuronal migration and a smooth brain phenotype known as lissencephaly. <jats:italic>Lis1<\/jats:italic><jats:sup>+\/\u2212<\/jats:sup> (<jats:italic>Pafah1b1<\/jats:italic>) mice show defective lamination in the cerebral cortex and hippocampal formation, whereas homozygous mutations result in embryonic lethality. Given that Lis1 is highly expressed in embryonic neurons, we hypothesized that sympathetic and parasympathetic preganglionic neurons (SPNs and PPNs) would exhibit migratory defects in <jats:italic>Lis1<\/jats:italic><jats:sup>+\/\u2212<\/jats:sup> mice. The initial radial migration of SPNs and PPNs that occurs together with somatic motor neurons appeared unaffected in <jats:italic>Lis1<\/jats:italic><jats:sup>+\/\u2212<\/jats:sup> mice. The subsequent dorsally directed tangential migration, however, was aberrant in a subset of these neurons. At all embryonic ages analyzed, the distribution of SPNs and PPNs in <jats:italic>Lis1<\/jats:italic><jats:sup>+\/\u2212<\/jats:sup> mice was elongated dorsoventrally compared with <jats:italic>Lis1<\/jats:italic><jats:sup>+\/+<\/jats:sup> mice. Individual cell bodies of ectopic preganglionic neurons were found in the ventral spinal cord with their leading processes oriented along their dorsal migratory trajectory. By birth, <jats:italic>Lis1<\/jats:italic><jats:sup>+\/\u2212<\/jats:sup> SPNs and PPNs were separated into distinct groups, those that were correctly, and those incorrectly positioned in the intermediate horn. As mispositioned SPNs and PPNs still were detected in P30 <jats:italic>Lis1<\/jats:italic><jats:sup>+\/\u2212<\/jats:sup> mice, we conclude that these neurons ceased migration prematurely. Additionally, we found that a dorsally located group of somatic motor neurons in the lumbar spinal cord, the retrodorsolateral nucleus, showed delayed migration in <jats:italic>Lis1<\/jats:italic><jats:sup>+\/\u2212<\/jats:sup> mice. These results suggest that <jats:italic>Lis1<\/jats:italic> is required for the dorsally directed tangential migration of many sympathetic and parasympathetic preganglionic neurons and a subset of somatic motor neurons. J. Comp. Neurol. 520:1198\u20131211, 2012. \u00a9 2011 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/cne.22768","type":"journal-article","created":{"date-parts":[[2011,9,20]],"date-time":"2011-09-20T19:11:43Z","timestamp":1316545903000},"page":"1198-1211","source":"Crossref","is-referenced-by-count":5,"title":["Lis1 reduction causes tangential migratory errors in mouse spinal cord"],"prefix":"10.1002","volume":"520","author":[{"given":"Katherine D.","family":"Moore","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Renee","family":"Chen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marianne","family":"Cilluffo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeffrey A.","family":"Golden","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Patricia 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