Syntaphilin-Mediated Docking of Mitochondria at the Growth Cone Is Dispensable for Axon Elongation<i>In Vivo</i>

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書誌事項

公開日
2019-09
資源種別
journal article
権利情報
  • https://creativecommons.org/licenses/by-nc-sa/4.0/
DOI
  • 10.1523/eneuro.0026-19.2019
公開者
Society for Neuroscience

説明

<jats:title>Abstract</jats:title><jats:p>Mitochondria are abundantly detected at the growth cone, the dynamic distal tip of developing axons that directs growth and guidance. It is, however, poorly understood how mitochondrial dynamics relate to growth cone behavior<jats:italic>in vivo</jats:italic>, and which mechanisms are responsible for anchoring mitochondria at the growth cone during axon pathfinding. Here, we show that in retinal axons elongating along the optic tract in zebrafish, mitochondria accumulate in the central area of the growth cone and are occasionally observed in filopodia extending from the growth cone periphery. Mitochondrial behavior at the growth cone<jats:italic>in vivo</jats:italic>is dynamic, with mitochondrial positioning and anterograde transport strongly correlating with growth cone behavior and axon outgrowth. Using novel zebrafish mutant lines that lack the mitochondrial anchoring proteins Syntaphilin a and b, we further show that Syntaphilins contribute to mitochondrial immobilization at the growth cone. Syntaphilins are, however, not required for proper growth cone morphology and axon growth<jats:italic>in vivo</jats:italic>, indicating that Syntaphilin-mediated anchoring of mitochondria at the growth cone plays only a minor role in elongating axons.</jats:p>

収録刊行物

  • eneuro

    eneuro 6 (5), ENEURO.0026-19.2019, 2019-09

    Society for Neuroscience

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