{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T14:14:05Z","timestamp":1791036845897,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2003,6,16]],"date-time":"2003-06-16T00:00:00Z","timestamp":1055721600000},"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":[[2003,8,25]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The shaking rat Kawasaki (SRK) is an autosomal recessive mutant that exhibits <jats:italic>reeler<\/jats:italic>\u2010like abnormal locomotor behaviors. The murine <jats:italic>reeler<\/jats:italic> mutants arise from several mutations in the specific gene called <jats:italic>reelin<\/jats:italic>, which result in defects of Reelin expression or secretion in the cerebral cortex and other regions of CNS. To address the issue of whether the SRK mutation also arises from a mutation in <jats:italic>reelin<\/jats:italic>, we analyzed the <jats:italic>reelin<\/jats:italic> gene in SRK. Northern analysis of <jats:italic>reelin<\/jats:italic> mRNA from normal rats showed that rat <jats:italic>reelin<\/jats:italic> was expressed as a \u223c12\u2010kb transcript in both the cerebrum and the cerebellum, whereas <jats:italic>reelin<\/jats:italic> expression was markedly reduced in the SRK brains. In situ hybridization analysis showed that <jats:italic>reelin<\/jats:italic> mRNA in the SRK brains was expressed in Cajal\u2010Retzius cells in the marginal zone of the cerebral cortex and outer granular cells in the cerebellar cortex in similar manners to normal controls, but its expression was considerably reduced. On Western blotting and immunohistochemical analyses using antibodies specific for the Reelin protein, no immunoproduct was recognized in the cerebral and cerebellar cortices. From the cDNA sequences, we found a 64\u2010base heterologous sequence in SRK <jats:italic>reelin<\/jats:italic>, which contains a termination codon in the reading frame. Furthermore, genomic DNA analysis revealed that a 10\u2010base deletion, which contains a predicted splice donor site, occurred in the SRK genomic <jats:italic>reelin<\/jats:italic> gene, resulting in \u201cread through\u201d into the following intron in SRK. Thus, the SRK mutation is another type of mutation that lacks expression of the functional Reelin protein and, therefore, causes the <jats:italic>reeler<\/jats:italic> phenotype. J. Comp. Neurol. 463:303\u2013315, 2003. \u00a9 2003 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/cne.10761","type":"journal-article","created":{"date-parts":[[2003,6,18]],"date-time":"2003-06-18T10:13:02Z","timestamp":1055931182000},"page":"303-315","source":"Crossref","is-referenced-by-count":21,"title":["Missplicing resulting from a short deletion in the <i>reelin<\/i> gene causes <i>reeler<\/i>\u2010like neuronal disorders in the mutant shaking rat Kawasaki"],"prefix":"10.1002","volume":"463","author":[{"given":"Satoshi","family":"Kikkawa","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tatsuro","family":"Yamamoto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazuyo","family":"Misaki","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yayoi","family":"Ikeda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haruo","family":"Okado","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masaharu","family":"Ogawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter 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