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LIS-less neurons don't even make it to the starting gate

Laboratory of Developmental Neurobiology, The Rockefeller University, New York, NY 10021

Correspondence to Mary E. Hatten: hatten{at}rockefeller.edu

Abstract

The manuscript by Tsai et al. (935–945) is a tour de force analysis of a controversial issue in developmental neurobiology, namely the molecular basis of the devastating human brain malformation, type I lissencephaly (Lis1) (Jellinger, K., and A. Rett. 1976. Neuropadiatrie. 7:66–91). For several decades, defects in neuronal migration have been assumed to underlie all defects in cortical histogenesis. In the paper by Tsai et al., the authors use a variety of elegant approaches, including the first real-time imaging of cortical neurons with reduced levels of LIS1, to demonstrate that LIS1 and dynactin act as regulators of dynein during cortical histogenesis. A loss of LIS1 results in both a failure to exit the cortical germinal zone and abnormal neuronal process formation. Thus, the primary action of the mutation is to disrupt the production of neurons in the developing brain as well as their migration.

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