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First published online 16 April 2008
doi: 10.1242/dev.020693

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Zic2 promotes axonal divergence at the optic chiasm midline by EphB1-dependent and -independent mechanisms

¹ Instituto de Neurociencias de Alicante (Consejo Superior de Investigaciones Científicas-Universidad Miguel Hernández, CSIC-UMH). Campus San Juan, Avd. Ramón y Cajal s/n, Alicante 03550, Spain.
² Departments of Pathology and Cell Biology, Department of Neuroscience, Columbia University, College of Physicians and Surgeons, 630 W. 168th Street, New York, NY 10032, USA.

^* Author for correspondence (e-mail: e.herrera{at}umh.es)

Accepted 27 March 2008

Axons of retinal ganglion cells (RGCs) make a divergent choice at the optic chiasm to cross or avoid the midline in order to project to ipsilateral and contralateral targets, thereby establishing the binocular visual pathway. The zinc-finger transcription factor Zic2 and a member of the Eph family of receptor tyrosine kinases, EphB1, are both essential for proper development of the ipsilateral projection at the mammalian optic chiasm midline. Here, we demonstrate in mouse by functional experiments in vivo that Zic2 is not only required but is also sufficient to change the trajectory of RGC axons from crossed to uncrossed. In addition, our results reveal that this transcription factor regulates the expression of EphB1 in RGCs and also suggest the existence of an additional EphB1-independent pathway controlled by Zic2 that contributes to retinal axon divergence at the midline.

Key words: EphB1, Zic2, Binocular vision, Midline axon divergence, Mouse

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