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The Journal of Neuroscience, June 7, 2006, 26(23):6303-6313; doi:10.1523/JNEUROSCI.0332-06.2006

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Development/Plasticity/Repair
A Role for 1 Tubulin-Expressing Müller Glia in Regeneration of the Injured Zebrafish Retina

Blake V. Fausett and Daniel Goldman

The Molecular and Behavioral Neuroscience Institute and Department of Biological Chemistry, University of Michigan, Ann Arbor, Michigan 48109

Correspondence should be addressed to Daniel Goldman, University of Michigan, Molecular and Behavioral Neuroscience Institute, Biomedical Sciences Research Building, 109 Zina Pitcher Place, Ann Arbor, MI 48109. Email: neuroman{at}umich.edu

1 tubulin (1T) is a neuron-specific microtubule protein whose expression is induced in the developing and regenerating CNS. In the adult CNS, 1T expression remains high in neural progenitors. Transgenic zebrafish harboring a 1.7 kb 1T promoter fragment along with the first exon and intron express the transgene in a manner that recapitulates expression of the endogenous gene. We recently showed that this promoter mediates gene induction in retinal ganglion cells during optic nerve regeneration and in a subset of Müller glia that proliferate after retinal injury (Senut et al., 2004). To further characterize these Müller glia, we generated transgenic fish harboring an 1T promoter fragment that is specifically induced in these cells after retinal damage. Transgene expression, bromodeoxyuridine (BrdU) labeling, and stem cell marker expression suggested that 1T-expressing Müller glia dedifferentiate and become multipotent in response to injury. In addition, green fluorescent protein and BrdU-mediated lineage tracing combined with retinal gene expression analysis indicated that 1T-expressing Müller glia were capable of generating retinal neurons and glia. These data strongly suggest 1T-expressing Müller glia dedifferentiate and mediate regeneration of the injured zebrafish retina.

Key words: Müller glia; stem cells; regeneration; retina; zebrafish; tubulin

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Received Sept. 23, 2005; revised April 25, 2006; accepted May 6, 2006.

Correspondence should be addressed to Daniel Goldman, University of Michigan, Molecular and Behavioral Neuroscience Institute, Biomedical Sciences Research Building, 109 Zina Pitcher Place, Ann Arbor, MI 48109. Email: neuroman{at}umich.edu

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