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Nucleic Acids Research Advance Access published online on December 17, 2007
Nucleic Acids Research, doi:10.1093/nar/gkm1099
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© 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

Dlx2 homeobox gene transcriptional regulation of Trkb neurotrophin receptor expression during mouse retinal development

Jimmy de Melo1, Qing-Ping Zhou2, Qi Zhang1, Shunzhen Zhang2,3, Mario Fonseca1,2, Jeffrey T. Wigle4,5 and David D. Eisenstat1–4,6,*

1Department of Human Anatomy and Cell Science, 2Manitoba Institute of Cell Biology, 3Department of Pediatrics and Child Health, 4Department of Biochemistry and Medical Genetics, 5St Boniface General Hospital Research Centre and 6Department of Ophthalmology, University of Manitoba, Winnipeg, Manitoba, Canada R3E 0V9

*To whom correspondence should be addressed. Tel: 204 787 1169; Fax: 204 787 2190; Email: eisensta{at}cc.umanitoba.ca

Received October 4, 2007. Revised November 25, 2007. Accepted November 25, 2007.

Dlx homeobox genes are first expressed in embryonic retina at E11.5. The Dlx1/Dlx2 null retina has a reduced ganglion cell layer (GCL), with loss of late-born differentiated retinal ganglion cells (RGCs) due to increased apoptosis. TrkB signaling is proposed to regulate the dynamics of RGC apoptosis throughout development. DLX2 expression markedly precedes the onset of TrkB expression in the GCL; TrkB co-expression with Dlx2 and RGC markers is well-established by E13.5. In the Dlx1/Dlx2 null retina, TrkB expression is significantly reduced by E16.5. We demonstrated that DLX2 binds to a specific region of the TrkB promoter in retinal neuroepithelium during embryogenesis. In vitro confirmation and the functional consequences of DLX2 binding to this TrkB regulatory region support TrkB as a Dlx2 transcriptional target. Furthermore, ectopic Dlx2 expression in retinal explants activates TrkB expression and Dlx2 knockdown in primary retinal cultures results in reduced TrkB expression. RGC differentiation and survival require the coordinated expression of transcription factors. This study establishes a direct transcriptional relationship between a homeodomain protein involved in RGC differentiation and a neurotrophin receptor implicated in RGC survival. Signaling mediated by TrkB may contribute to survival of late-born RGCs whose terminal differentiation is regulated by Dlx gene function.


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