Drosophila Lis1 is required for neuroblast proliferation, dendritic elaboration and axonal transport.
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.
Liu
Z
Z
Department of Biological Sciences, Stanford University, Stanford, California 94305-5020, USA.
Steward
R
R
Luo
L
L
D000818:Animals; D030801:Animals, Genetically Modified; D001370:Axonal Transport / Q000502:physiology*; D002454:Cell Differentiation; D002455:Cell Division; D002490:Central Nervous System / Q000196:embryology / Q000378:metabolism; D003712:Dendrites / Q000502:physiology*; D004330:Drosophila; D029721:Drosophila Proteins; D008869:Microtubule-Associated Proteins / Q000235:genetics / Q000378:metabolism* / Q000502:physiology; D016296:Mutagenesis; D009474:Neurons / Q000502:physiology*
D029721:Drosophila Proteins; C513192:Lis-1 protein, Drosophila; D008869:Microtubule-Associated Proteins