Slit1 and Slit2 cooperate to prevent premature midline crossing of retinal axons in the mouse visual system
Slit1 and Slit2 cooperate to prevent premature midline crossing of retinal axons in the mouse visual system
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DOI：
10.1016/s0896-6273(01)00586-4
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发表时间：
2002-01-17
期刊：
影响因子：
16.2
通讯作者：
Tessier-Lavigne, M
中科院分区：
文献类型：
--
作者：
Plump, AS;Erskine, L;Tessier-Lavigne, M
在发育过程中，视网膜神经节细胞(RGC)轴突穿过或避开视交叉的中线。在果蝇中，Sit蛋白通过排斥来调节中线轴突的交叉。为了确定Sit蛋白在RGC轴突引导中的作用，我们中断了Slit1和Slit2，这是已知的三个小鼠Slit1基因中的两个。单独缺失这两个基因的小鼠几乎没有表现出RGC轴突引导缺陷，但在双突变小鼠中，在真正的交叉之前出现了大量额外的交叉，许多视网膜轴突投射到对侧视神经，一些延伸到交叉的异位背侧。我们的结果表明，Sit蛋白在体内排斥视网膜轴突，并协同建立轴突通道，从而帮助确定腹侧间脑中形成视交叉的位置。
During development, retinal ganglion cell (RGC) axons either cross or avoid the midline at the optic chiasm. In Drosophila, the Slit protein regulates midline axon crossing through repulsion. To determine the role of Slit proteins in RGC axon guidance, we disrupted Slit1 and Slit2, two of three known mouse Slit genes. Mice defective in either gene alone exhibited few RGC axon guidance defects, but in double mutant mice a large additional chiasm developed anterior to the true chiasm, many retinal axons projected into the contralateral optic nerve, and some extended ectopically-dorsal and lateral to the chiasm. Our results indicate that Slit proteins repel retinal axons in vivo and cooperate to establish a corridor through which the axons are channeled, thereby helping define the site in the ventral diencephalon where the optic chiasm forms.