β-Catenin inactivation is a pre-requisite for chick retina regeneration

In the present study we explored the role of β-catenin in mediating chick retina regeneration. The chick can regenerate its retina by activating stem/progenitor cells present in the ciliary margin (CM) of the eye or via transdifferentiation of the retinal pigmented epithelium (RPE). Both modes requi...

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Bibliographic Details
Published in:PloS one 2014-07, Vol.9 (7), p.e101748
Main Authors: Zhu, Jie, Luz-Madrigal, Agustin, Haynes, Tracy, Zavada, Julia, Burke, Amy K, Del Rio-Tsonis, Katia
Format: Article
Language:English
Subjects:
Animals
beta Catenin - genetics
beta Catenin - metabolism
Biology
Biology and Life Sciences
Cell adhesion & migration
Cell cycle
Cell Differentiation
Cell growth
Cell Nucleus - metabolism
Cell Proliferation
Cells (biology)
Chick Embryo
Deactivation
Epithelium
Eye injuries
Fibroblast growth factor 2
Fibroblast Growth Factor 2 - pharmacology
Fibroblast growth factors
Gene Expression
Gene Expression Regulation, Developmental - drug effects
Heterocyclic Compounds, 3-Ring - pharmacology
Immunohistochemistry
Inactivation
Injury prevention
Kinases
LEF protein
Lymphoid Enhancer-Binding Factor 1 - genetics
Lymphoid Enhancer-Binding Factor 1 - metabolism
Phenotype
Phosphorylation
Progenitor cells
Protein Transport
Proteins
Regeneration
Research and Analysis Methods
Retina
Retina - cytology
Retina - drug effects
Retina - embryology
Retina - physiology
Retinal pigment epithelium
Retinal Pigment Epithelium - embryology
Retinal Pigment Epithelium - physiology
Signaling
SOXB1 Transcription Factors - genetics
SOXB1 Transcription Factors - metabolism
Stem cells
TCF Transcription Factors - genetics
TCF Transcription Factors - metabolism
Transcription, Genetic
Wnt Signaling Pathway - drug effects
Xenopus
β-Catenin
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Summary:In the present study we explored the role of β-catenin in mediating chick retina regeneration. The chick can regenerate its retina by activating stem/progenitor cells present in the ciliary margin (CM) of the eye or via transdifferentiation of the retinal pigmented epithelium (RPE). Both modes require fibroblast growth factor 2 (FGF2). We observed, by immunohistochemistry, dynamic changes of nuclear β-catenin in the CM and RPE after injury (retinectomy). β-Catenin nuclear accumulation was transiently lost in cells of the CM in response to injury alone, while the loss of nuclear β-catenin was maintained as long as FGF2 was present. However, nuclear β-catenin positive cells remained in the RPE in response to injury and were BrdU-/p27+, suggesting that nuclear β-catenin prevents those cells from entering the cell cycle. If FGF2 is present, the RPE undergoes dedifferentiation and proliferation concomitant with loss of nuclear β-catenin. Moreover, retinectomy followed by disruption of active β-catenin by using a signaling inhibitor (XAV939) or over-expressing a dominant negative form of Lef-1 induces regeneration from both the CM and RPE in the absence of FGF2. Our results imply that β-catenin protects cells of the CM and RPE from entering the cell cycle in the developing eye, and specifically for the RPE during injury. Thus inactivation of β-catenin is a pre-requisite for chick retina regeneration.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0101748