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Zic2通过依赖EphB1和不依赖EphB1的机制促进视交叉中线处的轴突发散。

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

作者信息

García-Frigola Cristina, Carreres Maria Isabel, Vegar Celia, Mason Carol, Herrera Eloísa

机构信息

Consejo Superior de Investigaciones Científicas-Universidad Miguel Hernández, CSIC-UMH Juan, Avd. Ramón y Cajal s/n, Alicante 03550, Spain.

出版信息

Development. 2008 May;135(10):1833-41. doi: 10.1242/dev.020693. Epub 2008 Apr 16.

DOI:10.1242/dev.020693
PMID:18417618
Abstract

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.

摘要

视网膜神经节细胞(RGCs)的轴突在视交叉处做出不同的选择,即穿过或避开中线,以便投射到同侧和对侧目标,从而建立双眼视觉通路。锌指转录因子Zic2和受体酪氨酸激酶Eph家族成员EphB1,对于哺乳动物视交叉中线同侧投射的正常发育都是必不可少的。在这里,我们通过体内功能实验在小鼠中证明,Zic2不仅是必需的,而且足以改变RGC轴突从交叉到不交叉的轨迹。此外,我们的结果表明,这种转录因子调节RGCs中EphB1的表达,并且还表明存在由Zic2控制的另外一条不依赖EphB1的通路,该通路有助于视网膜轴突在中线处的发散。

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