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

A. S. Plump, Lynda Erskine, C. Sabatier, K. Brose, C. J. Epstein, C. S. Goodman, C. A. Mason, M. Tessier-Lavigne

Research output: Contribution to journalArticle

318 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)219-232
Number of pages13
JournalNeuron
Volume33
Issue number2
DOIs
Publication statusPublished - 17 Jan 2002

Keywords

  • ganglion-cell axons
  • growth cone behavior
  • optic chiasm
  • chondrotin sulfate
  • neuronal migration
  • uncrossed axons
  • ephrina ligands
  • vertebrate slit
  • nervous-system
  • guidance

Cite this

Plump, A. S., Erskine, L., Sabatier, C., Brose, K., Epstein, C. J., Goodman, C. S., ... Tessier-Lavigne, M. (2002). Slit1 and Slit2 cooperate to prevent premature midline crossing of retinal axons in the mouse visual system. Neuron, 33(2), 219-232. https://doi.org/10.1016/S0896-6273(01)00586-4

Slit1 and Slit2 cooperate to prevent premature midline crossing of retinal axons in the mouse visual system. / Plump, A. S.; Erskine, Lynda; Sabatier, C.; Brose, K.; Epstein, C. J.; Goodman, C. S.; Mason, C. A.; Tessier-Lavigne, M.

In: Neuron, Vol. 33, No. 2, 17.01.2002, p. 219-232.

Research output: Contribution to journalArticle

Plump, AS, Erskine, L, Sabatier, C, Brose, K, Epstein, CJ, Goodman, CS, Mason, CA & Tessier-Lavigne, M 2002, 'Slit1 and Slit2 cooperate to prevent premature midline crossing of retinal axons in the mouse visual system' Neuron, vol. 33, no. 2, pp. 219-232. https://doi.org/10.1016/S0896-6273(01)00586-4
Plump, A. S. ; Erskine, Lynda ; Sabatier, C. ; Brose, K. ; Epstein, C. J. ; Goodman, C. S. ; Mason, C. A. ; Tessier-Lavigne, M. / Slit1 and Slit2 cooperate to prevent premature midline crossing of retinal axons in the mouse visual system. In: Neuron. 2002 ; Vol. 33, No. 2. pp. 219-232.
@article{41a771684ead452d9b9c0e90743afec5,
title = "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.",
keywords = "ganglion-cell axons, growth cone behavior, optic chiasm, chondrotin sulfate, neuronal migration, uncrossed axons, ephrina ligands, vertebrate slit, nervous-system, guidance",
author = "Plump, {A. S.} and Lynda Erskine and C. Sabatier and K. Brose and Epstein, {C. J.} and Goodman, {C. S.} and Mason, {C. A.} and M. Tessier-Lavigne",
note = "Previewed in: Neuron 33, 153-158. Highlighted in: Nat. Neurosci. Rev. 3, 168. Faculty of Biology “Must Read Paper”: http://www.f1000biology.com/article/id/1003701/evaluation",
year = "2002",
month = "1",
day = "17",
doi = "10.1016/S0896-6273(01)00586-4",
language = "English",
volume = "33",
pages = "219--232",
journal = "Neuron",
issn = "0896-6273",
publisher = "Cell Press",
number = "2",

}

TY - JOUR

T1 - Slit1 and Slit2 cooperate to prevent premature midline crossing of retinal axons in the mouse visual system

AU - Plump, A. S.

AU - Erskine, Lynda

AU - Sabatier, C.

AU - Brose, K.

AU - Epstein, C. J.

AU - Goodman, C. S.

AU - Mason, C. A.

AU - Tessier-Lavigne, M.

N1 - Previewed in: Neuron 33, 153-158. Highlighted in: Nat. Neurosci. Rev. 3, 168. Faculty of Biology “Must Read Paper”: http://www.f1000biology.com/article/id/1003701/evaluation

PY - 2002/1/17

Y1 - 2002/1/17

N2 - 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.

AB - 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.

KW - ganglion-cell axons

KW - growth cone behavior

KW - optic chiasm

KW - chondrotin sulfate

KW - neuronal migration

KW - uncrossed axons

KW - ephrina ligands

KW - vertebrate slit

KW - nervous-system

KW - guidance

U2 - 10.1016/S0896-6273(01)00586-4

DO - 10.1016/S0896-6273(01)00586-4

M3 - Article

VL - 33

SP - 219

EP - 232

JO - Neuron

JF - Neuron

SN - 0896-6273

IS - 2

ER -