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Thus, the present study aimed to generate and analyze a model mouse to clarify whether <jats:italic>Reln<\/jats:italic> deficiency is associated with the pathogenesis of schizophrenia.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A mouse line with a novel <jats:italic>RELN<\/jats:italic> exonic deletion (<jats:italic>Reln<\/jats:italic>\u2010del) was established using the CRISPR\/Cas9 method to elucidate the underlying molecular mechanism. Subsequently, general behavioral tests and histopathological examinations of the model mice were conducted and phenotypic analysis of the cerebellar granule cell migration was performed.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The phenotype of homozygous <jats:italic>Reln<\/jats:italic>\u2010del mice was similar to that of <jats:italic>reeler<\/jats:italic> mice with cerebellar atrophy, dysplasia of the cerebral layers, and abrogated protein levels of cerebral reelin. The expression of reelin in heterozygous <jats:italic>Reln<\/jats:italic>\u2010del mice was approximately half of that in wild\u2010type mice. Conversely, behavioral analyses in heterozygous <jats:italic>Reln<\/jats:italic>\u2010del mice without cerebellar atrophy or dysplasia showed abnormal social novelty in the three\u2010chamber social interaction test. <jats:italic>In vitro<\/jats:italic> reaggregation formation and neuronal migration were severely altered in the cerebellar cultures of homozygous <jats:italic>Reln<\/jats:italic>\u2010del mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The present results in novel <jats:italic>Reln<\/jats:italic>\u2010del mice modeled after our patient with a novel exonic deletion in <jats:italic>RELN<\/jats:italic> are expected to contribute to the development of reelin\u2010based therapies for schizophrenia.<\/jats:p><\/jats:sec>","DOI":"10.1111\/pcn.12993","type":"journal-article","created":{"date-parts":[[2020,2,17]],"date-time":"2020-02-17T15:48:31Z","timestamp":1581954511000},"page":"318-327","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Generation and analysis of novel <i>Reln\u2010<\/i>deleted mouse model corresponding to exonic <i>Reln<\/i> deletion in schizophrenia"],"prefix":"10.1111","volume":"74","author":[{"given":"Masahito","family":"Sawahata","sequence":"first","affiliation":[{"name":"Department of Neuropsychopharmacology and Hospital Pharmacy Nagoya University, Graduate School of Medicine  Nagoya Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9072-2546","authenticated-orcid":false,"given":"Daisuke","family":"Mori","sequence":"additional","affiliation":[{"name":"Brain and Mind Research Center Nagoya University  Nagoya 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