CAMSAP3 maintains neuronal polarity through regulation of microtubule stability

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  • Varisa Pongrakhananon
    Laboratory for Cell Adhesion and Tissue Patterning, RIKEN Center for Developmental Biology/RIKEN Center for Biosystems Dynamics Research, 650-0047 Kobe, Japan;
  • Hiroko Saito
    Laboratory for Cell Adhesion and Tissue Patterning, RIKEN Center for Developmental Biology/RIKEN Center for Biosystems Dynamics Research, 650-0047 Kobe, Japan;
  • Sylvain Hiver
    Laboratory for Cell Adhesion and Tissue Patterning, RIKEN Center for Developmental Biology/RIKEN Center for Biosystems Dynamics Research, 650-0047 Kobe, Japan;
  • Takaya Abe
    Animal Resource Development Unit, RIKEN Center for Life Science Technologies, 650-0047 Kobe, Japan;
  • Go Shioi
    Genetic Engineering Team, RIKEN Center for Life Science Technologies, 650-0047 Kobe, Japan;
  • Wenxiang Meng
    State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, 100101 Beijing, China
  • Masatoshi Takeichi
    Laboratory for Cell Adhesion and Tissue Patterning, RIKEN Center for Developmental Biology/RIKEN Center for Biosystems Dynamics Research, 650-0047 Kobe, Japan;

Description

<jats:title>Significance</jats:title><jats:p>Each neuron forms a single axon and multiple dendrites, and this configuration is important for wiring the brain. How only a single axon extends from a neuron, however, remains unknown. This study demonstrates that CAMSAP3, a protein that binds the minus-end of microtubules, preferentially localizes along axons in hippocampal neurons. Remarkably, mutations of CAMSAP3 lead to production of multiple axons in these neurons. In attempts to uncover mechanisms underlying this abnormal axon extension, the authors found that CAMSAP3-anchored microtubules escape from acetylation, a process mediated by α-tubulin acetyltransferase-1, and depletion of this enzyme abolishes abnormal axon formation in CAMSAP3 mutants. These findings reveal that CAMSAP3 controls microtubule dynamics, preventing tubulin acetylation; this mechanism is required for single-axon formation.</jats:p>

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