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

Abstract:

: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.

journal_name

Neuron

journal_title

Neuron

authors

Plump AS,Erskine L,Sabatier C,Brose K,Epstein CJ,Goodman CS,Mason CA,Tessier-Lavigne M

doi

10.1016/s0896-6273(01)00586-4

subject

Has Abstract

pub_date

2002-01-17 00:00:00

pages

219-32

issue

2

eissn

0896-6273

issn

1097-4199

pii

S0896627301005864

journal_volume

33

pub_type

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