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Genetics of photoreceptor degeneration and regeneration in zebrafish

Zebrafish are unique in that they provide a useful model system for studying two critically important problems in retinal neurobiology, the mechanisms responsible for triggering photoreceptor cell death and the innate stem cell–mediated regenerative response elicited by this death. In this review we...

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Detalles Bibliográficos
Autores principales: Brockerhoff, Susan E., Fadool, James M.
Formato: Texto
Lenguaje:English
Publicado: SP Birkhäuser Verlag Basel 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3029675/
https://www.ncbi.nlm.nih.gov/pubmed/20972813
http://dx.doi.org/10.1007/s00018-010-0563-8
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author Brockerhoff, Susan E.
Fadool, James M.
author_facet Brockerhoff, Susan E.
Fadool, James M.
author_sort Brockerhoff, Susan E.
collection PubMed
description Zebrafish are unique in that they provide a useful model system for studying two critically important problems in retinal neurobiology, the mechanisms responsible for triggering photoreceptor cell death and the innate stem cell–mediated regenerative response elicited by this death. In this review we highlight recent seminal findings in these two fields. We first focus on zebrafish as a model for studying photoreceptor degeneration. We summarize the genes currently known to cause photoreceptor degeneration, and we describe the phenotype of a few zebrafish mutants in detail, highlighting the usefulness of this model for studying this process. In the second section, we discuss the several different experimental paradigms that are available to study regeneration in the teleost retina. A model outlining the sequence of gene expression starting from the dedifferentiation of Müller glia to the formation of rod and cone precursors is presented.
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spelling pubmed-30296752011-03-16 Genetics of photoreceptor degeneration and regeneration in zebrafish Brockerhoff, Susan E. Fadool, James M. Cell Mol Life Sci Review Zebrafish are unique in that they provide a useful model system for studying two critically important problems in retinal neurobiology, the mechanisms responsible for triggering photoreceptor cell death and the innate stem cell–mediated regenerative response elicited by this death. In this review we highlight recent seminal findings in these two fields. We first focus on zebrafish as a model for studying photoreceptor degeneration. We summarize the genes currently known to cause photoreceptor degeneration, and we describe the phenotype of a few zebrafish mutants in detail, highlighting the usefulness of this model for studying this process. In the second section, we discuss the several different experimental paradigms that are available to study regeneration in the teleost retina. A model outlining the sequence of gene expression starting from the dedifferentiation of Müller glia to the formation of rod and cone precursors is presented. SP Birkhäuser Verlag Basel 2010-10-24 2011 /pmc/articles/PMC3029675/ /pubmed/20972813 http://dx.doi.org/10.1007/s00018-010-0563-8 Text en © The Author(s) 2010 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
spellingShingle Review
Brockerhoff, Susan E.
Fadool, James M.
Genetics of photoreceptor degeneration and regeneration in zebrafish
title Genetics of photoreceptor degeneration and regeneration in zebrafish
title_full Genetics of photoreceptor degeneration and regeneration in zebrafish
title_fullStr Genetics of photoreceptor degeneration and regeneration in zebrafish
title_full_unstemmed Genetics of photoreceptor degeneration and regeneration in zebrafish
title_short Genetics of photoreceptor degeneration and regeneration in zebrafish
title_sort genetics of photoreceptor degeneration and regeneration in zebrafish
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3029675/
https://www.ncbi.nlm.nih.gov/pubmed/20972813
http://dx.doi.org/10.1007/s00018-010-0563-8
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