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Here, we report that heterozygous<jats:italic>yotari<\/jats:italic>mice harboring a single autosomal recessive<jats:italic>yotari<\/jats:italic>mutation of<jats:italic>Dab1<\/jats:italic>exhibited a thinner neocortical layer 1 than wild-type mice on postnatal day (P)7. However, a birth-dating study suggested that this reduction was not caused by failure of neuronal migration.<jats:italic>In utero<\/jats:italic>electroporation-mediated sparse labeling revealed that the superficial layer neurons of heterozygous<jats:italic>yotari<\/jats:italic>mice tended to elongate their apical dendrites within layer 2 than within layer 1. In addition, the CA1 pyramidal cell layer in the caudo-dorsal hippocampus was abnormally split in heterozygous<jats:italic>yotari<\/jats:italic>mice, and a birth-dating study revealed that this splitting was caused mainly by migration failure of late-born pyramidal neurons. Adeno-associated virus (AAV)-mediated sparse labeling further showed that many pyramidal cells within the split cell had misoriented apical dendrites. These results suggest that regulation of neuronal migration and positioning by Reelin-DAB1 signaling pathways has unique dependencies on<jats:italic>Dab1<\/jats:italic>gene dosage in different brain regions.<\/jats:p>","DOI":"10.1523\/eneuro.0433-22.2023","type":"journal-article","created":{"date-parts":[[2023,3,20]],"date-time":"2023-03-20T17:40:12Z","timestamp":1679334012000},"page":"ENEURO.0433-22.2023","source":"Crossref","is-referenced-by-count":8,"title":["Heterozygous<i>Dab1<\/i>Null Mutation Disrupts Neocortical and Hippocampal 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