Interaction of reelin signaling and Lis1 in brain development
作者： Amir H Assadi , Guangcheng Zhang , Uwe Beffert , Robert S McNeil , Amy L Renfro
DOI: 10.1038/NG1257
关键词: Hippocampal formation 、 Cell biology 、 Signal transduction 、 Neuronal migration disorder 、 Lissencephaly 、 Biology 、 Reelin 、 Reeler 、 PAFAH1B1 、 DAB1 、 Genetics
摘要: Loss-of-function mutations in RELN (encoding reelin) or PAFAH1B1 LIS1) cause lissencephaly, a human neuronal migration disorder. In the mouse, homozygous Reln result reeler phenotype, characterized by ataxia and disrupted cortical layers. Pafah1b1(+/-) mice have hippocampal layering defects, whereas mutants are embryonic lethal. encodes an extracellular protein that regulates layer formation interacting with VLDLR ApoER2 (Lrp8) receptors, thereby phosphorylating Dab1 signaling molecule. Lis1 associates microtubules modulates migration. We investigated interactions between reelin pathway brain development. Compound mutant disruptions heterozygous Pafah1b1 had higher incidence of hydrocephalus enhanced defects. bound reelin-induced phosphorylation-dependent manner. These data indicate genetic biochemical interaction Lis1.
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