April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
ß-catenin Signaling Is Downregulated In The Regenerating Zebrafish Retina
Author Affiliations & Notes
  • Ryne A. Gorsuch
    Department of Biology and Center for Zebrafish Research, University of Notre Dame, Notre Dame, Indiana
  • Michael Petravick
    Department of Biology and Center for Zebrafish Research, University of Notre Dame, Notre Dame, Indiana
  • David R. Hyde
    Department of Biology and Center for Zebrafish Research, University of Notre Dame, Notre Dame, Indiana
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 5995. doi:
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      Ryne A. Gorsuch, Michael Petravick, David R. Hyde; ß-catenin Signaling Is Downregulated In The Regenerating Zebrafish Retina. Invest. Ophthalmol. Vis. Sci. 2011;52(14):5995.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : The light-damaged zebrafish retina undergoes a robust regenerative response that initiates with Müller glia dividing asymmetrically to produce a proliferating neuronal progenitor cell (NPC) population that restores the lost neurons. In contrast, the damaged mammalian retina exhibits only a limited number of proliferating Müller glia that rarely differentiate into the proper cell type. However, treatment of the damaged rodent retinas with various growth factors can stimulate significantly more Müller glia to divide and increase the regeneration of the correct neuronal cell fate. Because Wnt ligands, which activate the canonical Wnt/ß-Catenin signaling pathway, appear to induce mammalian regeneration, we examined ß-Catenin expression in the regenerating zebrafish retina.

Methods: : The spatial and temporal expression of ß-Catenin during regeneration of the light-damaged retina was assessed by immunohistochemistry. ß-Catenin expression was also quantified from light-damaged retinal lysates by immunoblots. Quantitative real-time PCR (qRT-PCR) was used to analyze the expression of both ß-catenin paralogs (ctnnb1/2) during regeneration.

Results: : Prior to retinal damage, ß-Catenin was localized in INL nuclei, which likely represent subsets of Müller glia, bipolar and horizontal cells. At 31 hours of light, ß-Catenin expression was reduced in PCNA-positive INL cells, likely the proliferating Müller glia. ß-Catenin remains absent from PCNA-positive NPCs throughout the remainder of the light treatment. Furthermore, cytoplasmic expression of ß-Catenin increased at 51 hours of light and became strongly localized to the NPC cortical processes and the outer limiting membrane. Immunoblot analysis of total retinal lysate confirmed the increased ß-Catenin expression. qRT-PCR will reveal which ctnnb paralog is differentially expressed at the transcript level.

Conclusions: : Light-damage decreases ß-Catenin nuclear signaling in proliferating Müller glia, where it is redistributed to the cell cortex. In contrast to the mammalian retina, these data suggest that either ß-Catenin nuclear signaling must be downregulated for Müller glial proliferation or is needed to allow Müller glia to respond correctly to regenerative signals.

Keywords: proliferation • regeneration • signal transduction 
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