The Journal of Neuroscience, September 28, 2005, 25(39):8878-8888; doi:10.1523/JNEUROSCI.2005-05.2005
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Development/Plasticity/Repair
Calcium/Calmodulin-Dependent Protein Kinase II Alters Structural Plasticity and Cytoskeletal Dynamics in Drosophila
Ryan Andersen,
Yimei Li,
Mary Resseguie, and
Jay E. Brenman
Department of Cell and Developmental Biology and Neuroscience Center, University of North Carolina Chapel Hill, Chapel Hill, North Carolina 27599
Drosophila dendritic arborization (da) neurons contain subclasses of neurons with distinct dendritic morphologies. We investigated calcium/calmodulin-dependent protein kinase II (CaMKII) regulation of dendritic structure and dynamics in vivo using optically transparent Drosophila larvae. CaMKII increases the dynamic nature and formation of dendritic filopodia throughout larval development but only affects neurons that normally contain dendritic filopodia. In parallel, we examined the effects of Rac1 activity on dendritic structure to explore signaling specificity. In contrast to CaMKII activity, Rac1 does not alter filopodia stability but instead causes de novo filopodia formation on all da neurons. Although both mediators increase cytoskeletal turnover, measured by fluorescence recovery after photobleaching experiments, only CaMKII increases the dynamic nature of dendritic filopodia. CaMKII signaling thus appears to use mechanisms and machinery distinct from Rac1 signaling. This study illustrates a molecular means of uncoupling cytoskeletal regulation from morphological regulation. Our results suggest that Drosophila dendritic filopodia may share some cytoskeletal regulatory mechanisms with mammalian dendritic filopodia. Furthermore, general dendrite cytoskeletal compartmentalization is conserved in multipolar neurons.
Key words: actin; dendrites; Drosophila; filopodia; Rac1; CaMKII
Received Nov 5, 2004;
revised July 14, 2005;
accepted August 14, 2005.
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