New synaptic bouton formation is disrupted by misregulation of microtubule stability in aPKC mutants
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NeuroscienceDocument Type
Journal ArticlePublication Date
2004-05-26Keywords
Animals; Caenorhabditis elegans Proteins; Carrier Proteins; Cell Differentiation; Drosophila Proteins; Drosophila melanogaster; Glutamic Acid; *Intracellular Signaling Peptides and Proteins; Memory; Microfilaments; Microtubule-Associated Proteins; Microtubules; Mutation; Nerve Growth Factors; Nervous System; Neuronal Plasticity; Presynaptic Terminals; Protein Kinase C; Proteins; Synaptic TransmissionNeuroscience and Neurobiology
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The Baz/Par-3-Par-6-aPKC complex is an evolutionarily conserved cassette critical for the development of polarity in epithelial cells, neuroblasts, and oocytes. aPKC is also implicated in long-term synaptic plasticity in mammals and the persistence of memory in flies, suggesting a synaptic function for this cassette. Here we show that at Drosophila glutamatergic synapses, aPKC controls the formation and structure of synapses by regulating microtubule (MT) dynamics. At the presynapse, aPKC regulates the stability of MTs by promoting the association of the MAP1Brelated protein Futsch to MTs. At the postsynapse, aPKC regulates the synaptic cytoskeleton by controlling the extent of Actin-rich and MT-rich areas. In addition, we show that Baz and Par-6 are also expressed at synapses and that their synaptic localization depends on aPKC activity. Our findings establish a novel role for this complex during synapse development and provide a cellular context for understanding the role of aPKC in synaptic plasticity and memory.Source
Neuron. 2004 May 27;42(4):567-80.
DOI
10.1016/S0896-6273(04)00255-7Permanent Link to this Item
http://hdl.handle.net/20.500.14038/33197PubMed ID
15157419Related Resources
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