Slit1 and Slit2 cooperate to prevent premature midline crossing of retinal axons in the mouse visual system

被引:340
作者
Plump, AS
Erskine, L
Sabatier, C
Brose, K
Epstein, CJ
Goodman, CS
Mason, CA
Tessier-Lavigne, M
机构
[1] Univ Calif San Francisco, Howard Hughes Med Inst, Dept Anat, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Howard Hughes Med Inst, Dept Biochem & Biophys, San Francisco, CA 94143 USA
[3] Univ Calif San Francisco, Div Med Genet, San Francisco, CA 94143 USA
[4] Columbia Univ Coll Phys & Surg, Ctr Neurobiol & Behav, Dept Pathol, New York, NY 10032 USA
[5] Columbia Univ Coll Phys & Surg, Ctr Neurobiol & Behav, Dept Anat, New York, NY 10032 USA
[6] Columbia Univ Coll Phys & Surg, Ctr Neurobiol & Behav, Dept Cell Biol, New York, NY 10032 USA
[7] Univ Calif Berkeley, Howard Hughes Med Inst, Dept Mol & Cell Biol, Berkeley, CA 94720 USA
关键词
D O I
10.1016/S0896-6273(01)00586-4
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
引用
收藏
页码:219 / 232
页数:14
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