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Nucleic Acids Research Advance Access originally published online on September 25, 2007
Nucleic Acids Research 2007 35(19):6501-6516; doi:10.1093/nar/gkm608
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Nucleic Acids Research, 2007, Vol. 35, No. 19 6501-6516
© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

Generation of a transgenic zebrafish model of Tauopathy using a novel promoter element derived from the zebrafish eno2 gene

Qing Bai1,2, Jessica A. Garver1,2, Neil A. Hukriede3 and Edward A. Burton1–5,*

1Pittsburgh Institute for Neurodegenerative Diseases, 2Department of Neurology, 3Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, 4Department of Neurology, Pittsburgh VA Healthcare System and 5Division of Movement Disorders, University of Pittsburgh Medical Center, Pittsburgh, PA, USA

*To whom correspondence should be addressed. Tel: +1 4126488480; Fax: +1 4126489082; Email: eab25{at}pitt.edu

Received May 8, 2007. Revised July 25, 2007. Accepted July 26, 2007.

The aim of this study was to isolate cis-acting regulatory elements for the generation of transgenic zebrafish models of neurodegeneration. Zebrafish enolase-2 (eno2) showed neuronal expression increasing from 24 to 72 h post-fertilization (hpf) and persisting through adulthood. A 12 kb eno2 genomic fragment, extending from 8 kb upstream of exon 1 to exon 2, encompassing intron 1, was sufficient to drive neuronal reporter gene expression in vivo over a similar time course. Five independent lines of stable Tg(eno2 : GFP) zebrafish expressed GFP widely in neurons, including populations with relevance to neurodegeneration, such as cholinergic neurons, dopaminergic neurons and cerebellar Purkinje cells. We replaced the exon 2-GFP fusion gene with a cDNA encoding the 4-repeat isoform of the human microtubule-associated protein Tau. The first intron of eno2 was spliced with high fidelity and efficiency from the chimeric eno2-Tau transcript. Tau was expressed at ~8-fold higher levels in Tg(eno2 : Tau) zebrafish brain than normal human brain, and localized to axons, neuropil and ectopic neuronal somatic accumulations resembling neurofibrillary tangles. The 12 kb eno2 promoter drives high-level transgene expression in differentiated neurons throughout the CNS of stable transgenic zebrafish. This regulatory element will be useful for the construction of transgenic zebrafish models of neurodegeneration.


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