May 2004
Volume 45, Issue 13
ARVO Annual Meeting Abstract  |   May 2004
Retinal injury induces the expression of alpha–1 tubulin in teleost retinal progenitors
Author Affiliations & Notes
  • A.A. Sieh
    Neuroscience Graduate Program,
    University of Michigan, Ann Arbor, MI
  • D. Goldman
    Biological Chemistry, Mental Health Research Institute, University of Michigan, Ann Arbor, MI
  • P. Hitchcock
    Ophtalmology and Visual Sciences, Neuroscience Graduate Program , Kellog Eye Center,
    University of Michigan, Ann Arbor, MI
  • Footnotes
    Commercial Relationships  A.A. Sieh, None; D. Goldman, None; P. Hitchcock, None.
  • Footnotes
    Support  Support NIH Grant EY07060, EY07003, Support Training Grant T32–DC05341
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 5399. doi:
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      A.A. Sieh, D. Goldman, P. Hitchcock; Retinal injury induces the expression of alpha–1 tubulin in teleost retinal progenitors . Invest. Ophthalmol. Vis. Sci. 2004;45(13):5399.

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

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Abstract: : Purpose:Teleost fish have the capacity to regenerate their retinal neurons following injury. Molecular mechanisms involved in regulating this regenerative process are poorly understood. The study reported here sought to identify genes whose expressions are modulated during retinal regeneration. Alpha–1 tubulin is a member of the α–tubulin multigene family and is known to be expressed in neural progenitors. Expression of α–1 tubulin was analyzed following retinal injury. Methods:Two different species of teleost were used in this study: zebrafish, transgenic for green fluorescent protein (GFP) under the control of a specific α–1 tubulin promoter and common goldfish. Retinas were injured and fish were allowed to recover for various intervals. Prior to sacrifice animals were housed for 12–36 hrs. in a solution of 5mM BrdU to label proliferating cells. Eyecups were harvested and processed, according to standard techniques, for GFP and BrdU immunocytochemistry and in situ hybridization. Results:In the transgenic zebrafish, four days after retinal injury intense GFP expression was noted in the proliferative blastema. Cells expressing both GFP and BrdU were found to span all the retinal layers, with the majority being located in the inner nuclear layer (INL). In situ hybridization of adjacent sections with the α1–tubulin specific probe confirmed the specificity of the GFP signal, showing the upregulation of α1–tubulin in the mitotically active cells of the blastema. In the goldfish retina, ten days after injury, in situ hybridization revealed a robust expression of α1–tubulin at the margins of the retinal wound, corresponding to BrdU labeled retinal progenitors. In addition α1–tubulin expression was noted in cells close to the retinal lesion, some of which did not incorporate BrdU. Conclusions:These data show that α1–tubulin is robustly increased upon injury in retinal progenitors of both zebrafish and goldfish retinas. In the teleost retina α1–tubulin can thus be used as a molecular marker for injury induced retinal progenitors.

Keywords: regeneration • proliferation • gene/expression 

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