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. 2019 Mar 14;9:4420. doi: 10.1038/s41598-019-40734-z

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Model displaying the response of niche-specific stem/progenitor populations following lesion to the adult optic tectum. Top: Quiescent radial-glia (qRG) are unable to produce cycling progenitors under homeostasis at the tectal ventricle. Post-injury, a subpopulation of qRG transition to a proliferative state (pRG) to produce newly cycling progenitors which differentiate into de novo radial-glia (N-RG). Bottom: Neuro-epithelial-like amplifying progenitors (NE-Ap) are constitutively active under homeostasis, acting as a lifelong source of newborn neurons (N-Neu) at the internal tectal marginal zone (TMZi). Tectal injury induces NE-Ap to increase their homeostatic level of cell proliferation, leading to an increase in neuronal output to replace neurons lost to damage. This regenerative process is associated with an increase in Wnt/β-catenin signalling. TeO, tectum opticum; PGZ, periventricular grey zone.