Syntaphilin-mediated docking of mitochondria at the growth cone is dispensable for axon elongation in vivo

Verreet, T., Weaver, C.J., Hino, H., Hibi, M., Poulain, F.E.
eNeuro   6(5): (Journal)
Registered Authors
Hibi, Masahiko, Hino, Hiromu, Poulain, Fabienne
axon growth, confocal live imaging, mitochondria, syntaphilin, visual system, zebrafish
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Axons/physiology*
  • Growth Cones/physiology*
  • Membrane Proteins/physiology*
  • Mitochondria/physiology*
  • Nerve Tissue Proteins/physiology*
  • Neuronal Outgrowth/physiology*
  • Zebrafish
31481398 Full text @ eNeuro
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 in vivo, 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 in vivo 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 in vivo, indicating that Syntaphilin-mediated anchoring of mitochondria at the growth cone only plays a minor role in elongating axons.Significance statement Proper axon elongation and pathfinding are essential for nervous system wiring. The growth cone, a dynamic structure at the distal end of axons, mediates axonal growth and guidance. Here, we describe for the first time in vivo the behavior of mitochondria at the growth cone of elongating axons. We show that mitochondria accumulate in the growth cone central area and are also present in its periphery. We further provide evidence that Syntaphilin, which immobilizes mitochondria along mature axons, also docks mitochondria at the growth cone. However, loss of Syntaphilin did not cause a complete depletion of mitochondria from the growth cone and did not affect axon elongation, indicating that other mitochondria-docking factors regulate axon growth during development.
Genes / Markers
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Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes