Abstract
Haplo-insufficiency of human Lis1 causes lissencephaly. Reduced Lis1 activity in both humans and mice results in a neuronal migration defect. Here we show that Drosophila Lis1 is highly expressed in the nervous system. Lis1 is essential for neuroblast proliferation and axonal transport, as shown by a mosaic analysis using a Lis1 null mutation. Moreover, it is cell-autonomously required for dendritic growth, branching and maturation. Analogous mosaic analysis shows that neurons containing a mutated cytoplasmic-dynein heavy chain (Dhc64C) exhibit phenotypes similar to Lis1 mutants. These results implicate Lis1 as a regulator of the microtubule cytoskeleton and show that it is important for diverse physiological functions in the nervous system.
Original language | English (US) |
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Pages (from-to) | 776-783 |
Number of pages | 8 |
Journal | Nature Cell Biology |
Volume | 2 |
Issue number | 11 |
DOIs | |
State | Published - 2000 |
All Science Journal Classification (ASJC) codes
- Cell Biology