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¹ Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, NY 10032
² Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, NY 10032
³ Center for Neurobiology and Behavior, College of Physicians and Surgeons, Columbia University, New York, NY 10032

Correspondence to Richard B. Vallee: rv2025{at}columbia.edu

Mutations in the human LIS1 gene cause the smooth brain disease classical lissencephaly. To understand the underlying mechanisms, we conducted in situ live cell imaging analysis of LIS1 function throughout the entire radial migration pathway. In utero electroporation of LIS1 small interference RNA and short hairpin dominant negative LIS1 and dynactin cDNAs caused a dramatic accumulation of multipolar progenitor cells within the subventricular zone of embryonic rat brains. This effect resulted from a complete failure in progression from the multipolar to the migratory bipolar state, as revealed by time-lapse analysis of brain slices. Surprisingly, interkinetic nuclear oscillations in the radial glial progenitors were also abolished, as were cell divisions at the ventricular surface. Those few bipolar cells that reached the intermediate zone also exhibited a complete block in somal translocation, although, remarkably, process extension persisted. Finally, axonal growth also ceased. These results identify multiple distinct and novel roles for LIS1 in nucleokinesis and process dynamics and suggest that nuclear position controls neural progenitor cell division.

A.R. Kriegstein's present address is Program in Developmental and Stem Cell Biology, University of California, San Francisco, San Francisco, CA 94143.

Abbreviations used in this paper: CP, cortical plate; IZ, intermediate zone; RNAi, RNA interference; shRNA, short hairpin RNA; siRNA, small interference RNA; SVZ, subventricular zone; VZ, ventricular zone.

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