LIS-less neurons fall behind

LIS1, the protein that is affected in the developmental disorder Lissencephaly, interacts with cytoplasmic dynein in several cell systems. As neuronal positioning is disrupted by this disease, LIS1 and dynein are assumed to be involved in neuronal migration. Now, live in vivo images from Tsai et al. (page 935) reveal that migration is just one facet of LIS1 function.

Neuronal development was blocked at multiple stages following the loss of LIS1, probably depending on the efficiency of RNAi uptake in a cell. The earliest defect was seen in the proliferation of neural progenitors. The nuclei of these precursors normally oscillate in the neural tube and divide when they reach the ventricular surface. But nuclei of cells lacking LIS1 did not oscillate and never divided. The authors suspect that...