par Fuss, Stefan H.;Kocagöz, Yigit;Eski, Sema Elif
Référence Annual Meeting of the European Chemoreception Research Organization (ECRO)(28th: 2018-09-01: Würzburg, Germany), Chemical senses, Chemical senses, Vol. 4, page (39)
Publication Publié, 2019-03-01
Publication dans des actes
Résumé : Olfactory sensory neurons (OSNs) have a limited life span and need to be generated constantly by maintenance neurogenesis to prevent olfactory loss at old age. In addition, the olfactory epithelium (OE) is capable of mounting efficient regenerative responses to acute tissue damage. In zebrafish, non-identical progenitor pools with distinct tissue distribution contribute to OSN maintenance and OE repair, however, the signals that regulate these two modes of OSN neurogenesis are not well characterized. We have used gene expression profiling by RNA sequencing to identify molecular signaling pathways that are significantly upregulated in an experimental model of OE regeneration. We find that components of the canonical Wnt/β-catenin signaling pathway are strongly activated early after damage to the OE. In the intact OE, β-catenin-positive cells are restricted to regions of maintenance neurogenesis at the central and peripheral edge of the sensory tissue, while repair neurogenesis is induced in the sensory OE upon damage. To test the contribution to Wnt/β-catenin signaling to these two modes of OSN neurogenesis functionally, we manipulated Wnt activity pharmacologically in the intact and lesioned OE. Activation of the Wnt pathway promoted strong cell proliferation responses, including responses in the sensory OE that resembled the pattern of neurogenesis under damage conditions. Inhibitors of the pathway, on the other hand, suppressed, but did not abolish, maintenance neurogenesis and had a suppressive effect on damage-induced proliferation in the sensory OE. Our results suggest that Wnt/β-catenin signaling is necessary and sufficient to induce cell proliferation from two types of neuronal progenitor populations in the OE that selectively contribute to maintenance and repair neurogenesis.