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Mol Cell Neurosci. 2017 Oct;84:29-35. doi: 10.1016/j.mcn.2017.07.006. Epub 2017 Jul 29.

How does calcium interact with the cytoskeleton to regulate growth cone motility during axon pathfinding?

Author information

1
School of Medicine, University of Tasmania, Hobart, Tasmania 7001, Australia. Electronic address: robert.gasperini@utas.edu.au.
2
School of Medicine, University of Tasmania, Hobart, Tasmania 7001, Australia. Electronic address: Macarena.Pavez@utas.edu.au.
3
School of Medicine, University of Tasmania, Hobart, Tasmania 7001, Australia. Electronic address: Adrian.Thompson@utas.edu.au.
4
Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania 7001, Australia. Electronic address: camilla.mitchell@petermac.org.
5
University of Exeter Medical School, Wellcome Wolfson Centre for Medical Research, Exeter EX2 5DW, United Kingdom. Electronic address: H.Hardy@exeter.ac.uk.
6
Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania 7001, Australia. Electronic address: kaylene.young@utas.edu.au.
7
University of Exeter Medical School, Wellcome Wolfson Centre for Medical Research, Exeter EX2 5DW, United Kingdom. Electronic address: J.K.Chilton@exeter.ac.uk.
8
School of Medicine, University of Tasmania, Hobart, Tasmania 7001, Australia. Electronic address: lisa.foa@utas.edu.au.

Abstract

The precision with which neurons form connections is crucial for the normal development and function of the nervous system. The development of neuronal circuitry in the nervous system is accomplished by axon pathfinding: a process where growth cones guide axons through the embryonic environment to connect with their appropriate synaptic partners to form functional circuits. Despite intense efforts over many years to understand how this process is regulated, the complete repertoire of molecular mechanisms that govern the growth cone cytoskeleton and hence motility, remain unresolved. A central tenet in the axon guidance field is that calcium signals regulate growth cone behaviours such as extension, turning and pausing by regulating rearrangements of the growth cone cytoskeleton. Here, we provide evidence that not only the amplitude of a calcium signal is critical for growth cone motility but also the source of calcium mobilisation. We provide an example of this idea by demonstrating that manipulation of calcium signalling via L-type voltage gated calcium channels can perturb sensory neuron motility towards a source of netrin-1. Understanding how calcium signals can be transduced to initiate cytoskeletal changes represents a significant gap in our current knowledge of the mechanisms that govern axon guidance, and consequently the formation of functional neural circuits in the developing nervous system.

KEYWORDS:

Actin; Axon guidance; Calcium; Cytoskeleton; Endoplasmic reticulum (ER); Growth cone; Microtubules

PMID:
28765051
DOI:
10.1016/j.mcn.2017.07.006
[Indexed for MEDLINE]
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