Anosmin-1a is required for fasciculation and terminal targeting of olfactory sensory neuron axons in the zebrafish olfactory system

Constantin Yanicostas , Eric Herbomel , Aurélie Dipietromaria , Nadia Soussi-Yanicostas

The gene underlies the Xlinked form of Kallmann syndrome (KS), a neurological disorder that impairs the development of the olfactory and GnRH systems. encodes anosmin1, a cell matrix protein that shows cell adhesion, neurite outgrowth, and axon-guidance and -branching activities. We used zebrafish embryos as model to better understand the role of this protein during olfactory system (OS) development. First, we detected the protein in olfactory sensory neurons from 22hours post-fertilization (hpf) onward, prior their pioneer axons reached presumptive olfactory bulbs (OBs). We found that anosmin-1a depletion impaired the fasciculation of olfactory axons and their terminal targeting within OBs. Last, we showed that inactivation induced a severe decrease in the number of GABAergic and dopaminergic OB neurons. Though the phenotypes induced following anosmin-1a depletion in zebrafish embryos did not match precisely the defects observed in KS patients, our results provide the first demonstration of a direct requirement for anosmin-1 in OS development in vertebrates and stress the role of OB innervation on OB neuron differentiation.

Mots clés: Anosmin-1; Kallmann syndrome; Olfactory system; Zebrafish; gene

Constantin Yanicostas, Eric Herbomel, Aurélie Dipietromaria, Nadia Soussi-Yanicostas. Anosmin-1a is required for fasciculation and terminal targeting of olfactory sensory neuron axons in the zebrafish olfactory system. Molecular and Cellular Endocrinology, 2009, 312 (1-2), pp.53. ⟨10.1016/j.mce.2009.04.017⟩. ⟨hal-00518309⟩