Retinal regeneration requires dynamic Notch signaling

Retinal damage in the adult zebrafish induces Müller glia reprogramming to produce neuronal progenitor cells that proliferate and differentiate into retinal neurons. Notch signaling, which is a fundamental mechanism known to drive cell-cell communication, is required to maintain Müller glia in a qui...

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Autores principales:	Leah J Campbell, Jaclyn L Levendusky, Shannon A Steines, David R Hyde
Formato:	article
Lenguaje:	EN
Publicado:	Wolters Kluwer Medknow Publications 2022
Materias:	differentiation; gliosis; müller glia; neuronal progenitor cell; notch signaling; proliferation; quiescence; retinal development; retinal regeneration; zebrafish Neurology. Diseases of the nervous system RC346-429
Acceso en línea:	https://doaj.org/article/f83c0fc6228f471da283d9edd793c166
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spelling	oai:doaj.org-article:f83c0fc6228f471da283d9edd793c1662021-11-19T12:16:44ZRetinal regeneration requires dynamic Notch signaling1673-537410.4103/1673-5374.327326https://doaj.org/article/f83c0fc6228f471da283d9edd793c1662022-01-01T00:00:00Zhttp://www.nrronline.org/article.asp?issn=1673-5374;year=2022;volume=17;issue=6;spage=1199;epage=1209;aulast=Campbellhttps://doaj.org/toc/1673-5374Retinal damage in the adult zebrafish induces Müller glia reprogramming to produce neuronal progenitor cells that proliferate and differentiate into retinal neurons. Notch signaling, which is a fundamental mechanism known to drive cell-cell communication, is required to maintain Müller glia in a quiescent state in the undamaged retina, and repression of Notch signaling is necessary for Müller glia to reenter the cell cycle. The dynamic regulation of Notch signaling following retinal damage also directs proliferation and neurogenesis of the Müller glia-derived progenitor cells in a robust regeneration response. In contrast, mammalian Müller glia respond to retinal damage by entering a prolonged gliotic state that leads to additional neuronal death and permanent vision loss. Understanding the dynamic regulation of Notch signaling in the zebrafish retina may aid efforts to stimulate Müller glia reprogramming for regeneration of the diseased human retina. Recent findings identified DeltaB and Notch3 as the ligand-receptor pair that serves as the principal regulators of zebrafish Müller glia quiescence. In addition, multi-omics datasets and functional studies indicate that additional Notch receptors, ligands, and target genes regulate cell proliferation and neurogenesis during the regeneration time course. Still, our understanding of Notch signaling during retinal regeneration is limited. To fully appreciate the complex regulation of Notch signaling that is required for successful retinal regeneration, investigation of additional aspects of the pathway, such as post-translational modification of the receptors, ligand endocytosis, and interactions with other fundamental pathways is needed. Here we review various modes of Notch signaling regulation in the context of the vertebrate retina to put recent research in perspective and to identify open areas of inquiry.Leah J CampbellJaclyn L LevenduskyShannon A SteinesDavid R HydeWolters Kluwer Medknow Publicationsarticledifferentiation; gliosis; müller glia; neuronal progenitor cell; notch signaling; proliferation; quiescence; retinal development; retinal regeneration; zebrafishNeurology. Diseases of the nervous systemRC346-429ENNeural Regeneration Research, Vol 17, Iss 6, Pp 1199-1209 (2022)
institution	DOAJ
collection	DOAJ
language	EN
topic	differentiation; gliosis; müller glia; neuronal progenitor cell; notch signaling; proliferation; quiescence; retinal development; retinal regeneration; zebrafish Neurology. Diseases of the nervous system RC346-429
spellingShingle	differentiation; gliosis; müller glia; neuronal progenitor cell; notch signaling; proliferation; quiescence; retinal development; retinal regeneration; zebrafish Neurology. Diseases of the nervous system RC346-429 Leah J Campbell Jaclyn L Levendusky Shannon A Steines David R Hyde Retinal regeneration requires dynamic Notch signaling
description	Retinal damage in the adult zebrafish induces Müller glia reprogramming to produce neuronal progenitor cells that proliferate and differentiate into retinal neurons. Notch signaling, which is a fundamental mechanism known to drive cell-cell communication, is required to maintain Müller glia in a quiescent state in the undamaged retina, and repression of Notch signaling is necessary for Müller glia to reenter the cell cycle. The dynamic regulation of Notch signaling following retinal damage also directs proliferation and neurogenesis of the Müller glia-derived progenitor cells in a robust regeneration response. In contrast, mammalian Müller glia respond to retinal damage by entering a prolonged gliotic state that leads to additional neuronal death and permanent vision loss. Understanding the dynamic regulation of Notch signaling in the zebrafish retina may aid efforts to stimulate Müller glia reprogramming for regeneration of the diseased human retina. Recent findings identified DeltaB and Notch3 as the ligand-receptor pair that serves as the principal regulators of zebrafish Müller glia quiescence. In addition, multi-omics datasets and functional studies indicate that additional Notch receptors, ligands, and target genes regulate cell proliferation and neurogenesis during the regeneration time course. Still, our understanding of Notch signaling during retinal regeneration is limited. To fully appreciate the complex regulation of Notch signaling that is required for successful retinal regeneration, investigation of additional aspects of the pathway, such as post-translational modification of the receptors, ligand endocytosis, and interactions with other fundamental pathways is needed. Here we review various modes of Notch signaling regulation in the context of the vertebrate retina to put recent research in perspective and to identify open areas of inquiry.
format	article
author	Leah J Campbell Jaclyn L Levendusky Shannon A Steines David R Hyde
author_facet	Leah J Campbell Jaclyn L Levendusky Shannon A Steines David R Hyde
author_sort	Leah J Campbell
title	Retinal regeneration requires dynamic Notch signaling
title_short	Retinal regeneration requires dynamic Notch signaling
title_full	Retinal regeneration requires dynamic Notch signaling
title_fullStr	Retinal regeneration requires dynamic Notch signaling
title_full_unstemmed	Retinal regeneration requires dynamic Notch signaling
title_sort	retinal regeneration requires dynamic notch signaling
publisher	Wolters Kluwer Medknow Publications
publishDate	2022
url	https://doaj.org/article/f83c0fc6228f471da283d9edd793c166
work_keys_str_mv	AT leahjcampbell retinalregenerationrequiresdynamicnotchsignaling AT jaclynllevendusky retinalregenerationrequiresdynamicnotchsignaling AT shannonasteines retinalregenerationrequiresdynamicnotchsignaling AT davidrhyde retinalregenerationrequiresdynamicnotchsignaling
_version_	1718420108585467904

Retinal regeneration requires dynamic Notch signaling

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