Interneuron migration from basal forebrain to neocortex: dependence on Dlx genes. The adhesion molecule TAG-1 mediates the migration of cortical interneurons from the ganglionic eminence along the corticofugal fiber system. Sorting of striatal and cortical interneurons regulated by semaphorin–neuropilin interactions. Marin, O., Yaron, A., Bagri, A., Tessier-Lavigne, M. In utero fate mapping reveals distinct migratory pathways and fates of neurons born in the mammalian basal forebrain. Wichterle, H., Turnbull, D.H., Nery, S., Fishell, G. The origin and migration of cortical neurones: new vistas. Induction and dorsoventral patterning of the telencephalon. Differential origins of neocortical projection and local circuit neurons: role of Dlx genes in neocortical interneurogenesis. Doublecortin is a microtubule-associated protein and is expressed widely by migrating neurons. Doublecortin is a developmentally regulated, microtubule-associated protein expressed in migrating and differentiating neurons. LIS1 regulates CNS lamination by interacting with mNudE, a central component of the centrosome. Regulation of cytoplasmic dynein behavior and microtubule organization by mammalian Lis1. A protein related to extracellular matrix proteins deleted in the mouse mutant reeler. Targeted mutagenesis of Lis1 disrupts cortical development and LIS1 homodimerization. Graded reduction of Pafah1b1 (Lis1) activity results in neuronal migration defects and early embryonic lethality. LIS1 and XLIS ( DCX) mutations cause most classical lissencephaly, but different patterns of malformation. Differences in the gyral pattern distinguish chromosome 17-linked and X-linked lissencephaly. Autosomal recessive lissencephaly with cerebellar hypoplasia is associated with human RELN mutations. Doublecortin, a brain-specific gene mutated in human X-linked lissencephaly and double cortex syndrome, encodes a putative signaling protein. A novel CNS gene required for neuronal migration and involved in X-linked subcortical laminar heteropia and lissencephaly syndrome. Isolation of a Miller–Dicker lissencephaly gene containing G protein β-subunit–like repeats. X-linked malformations of cortical development.
Pearlman, A.L., Faust, P.L., Hatten, M.E.
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