Robo1 and Robo2 Cooperate to Control the Guidance of Major Axonal Tracts in the Mammalian Forebrain

López‐Bendito, Guillermina; Flames, Nuria; Ma, Le; Fouquet, Coralie; Meglio, Thomas Di; Chédotal, Alain; Tessier‐Lavigne, Marc; Marı́n, Oscar

doi:10.1523/jneurosci.4605-06.2007

Cited by 207 publications

(228 citation statements)

References 50 publications

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“…To test this model, we analyzed the phenotype of Robo1, Robo2, Slit1, and Slit2 single and double knock-out mice. As shown previously, our Robo1 allele is likely to be a severe hypomorph rather than a complete null (Long et al, 2004;Lopez-Bendito et al, 2007). IO neurons were visualized using Brn3.2 immunostaining (Fig.…”

Section: Abnormal Migration Of Io Neurons Across the Floor Plate In Rsupporting

confidence: 55%

“…However, the Robo1 knock-out line used here was obtained by gene trap method and may be only be a hypomorphic allele (Long et al, 2004;Fouquet et al, 2007). Accordingly, their telencephalon has a milder phenotype than another line obtained by classic gene targeting method (Andrews et al, 2006;Lopez-Bendito et al, 2007). It would be important to compare the IO development of the two Robo1 lines.…”

Section: Discussionmentioning

confidence: 99%

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Molecular Mechanisms Controlling Midline Crossing by Precerebellar Neurons

Meglio¹,

Nguyen-Ba-Charvet²,

Tessier‐Lavigne³

et al. 2008

Journal of Neuroscience

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Precerebellar neurons of the inferior olive (IO) and lateral reticular nucleus (LRN) migrate tangentially from the rhombic lip toward the floor plate following parallel pathways. This process is thought to involve netrin-1 attraction. However, whereas the cell bodies of LRN neurons cross the midline, IO neurons are unable to do so. In many systems and species, axon guidance and cell migration at the midline are controlled by Slits and their receptor Robos. We showed previously that precerebellar axons and neurons do not cross the midline in the absence of the Robo3 receptor. To determine whether this signaling by Slits and the two other Robo receptors, Robo1 and Robo2, also regulates precerebellar neuron behavior at the floor plate, we studied the phenotype of Slit1/2 and Robo1/2/3 compound mutants. Our results showed that many IO neurons can cross the midline in absence of Slit1/2 or Robo1/2, supporting a role for midline repellents in guiding precerebellar neurons. We also show that these molecules control the development of the lamellation of the inferior olivary complex. Last, the analysis of Robo1/2/3 triple mutants suggests that Robo3 inhibits Robo1/2 repulsion in precrossing LRN axons but not in IO axons in which it has a dominant and distinct function.

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Section: Abnormal Migration Of Io Neurons Across the Floor Plate In Rsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Molecular Mechanisms Controlling Midline Crossing by Precerebellar Neurons

Meglio¹,

Nguyen-Ba-Charvet²,

Tessier‐Lavigne³

et al. 2008

Journal of Neuroscience

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“…9). Multiple axon guidance ligands and receptors regulate TCA development (5,6,8,(33)(34)(35). EphrinA5 is expressed within the VTel along a high-rostral to low-caudal gradient that maintains proper topographic organization of EphA-expressing TCAs from the rostro-medial thalamus to their rostral-cortical target regions (5).…”

Section: Discussionmentioning

confidence: 99%

EphB receptor forward signaling regulates area-specific reciprocal thalamic and cortical axon pathfinding

Robichaux

Chenaux

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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In early brain development, ascending thalamocortical axons (TCAs) navigate through the ventral telencephalon (VTel) to reach their target regions in the young cerebral cortex. Descending, deep-layer cortical axons subsequently target appropriate thalamic and subcortical target regions. However, precisely how and when corticothalamic axons (CTAs) identify their appropriate, reciprocal thalamic targets remains unclear. We show here that EphB1 and EphB2 receptors control proper navigation of a subset of TCA and CTA projections through the VTel. We show in vivo that EphB receptor forward signaling and the ephrinB1 ligand are required during the early navigation of L1-CAM + thalamic fibers in the VTel, and that the misguided thalamic fibers in EphB1/2 KO mice appear to interact with cortical subregion-specific axon populations during reciprocal cortical axon guidance. As such, our findings suggest that descending cortical axons identify specific TCA subpopulations in the dorsal VTel to coordinate reciprocal corticalthalamic connectivity in the early developing brain.

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“…Axonal defects develop because of a gain of polySia-negative NCAM, as they are not observed in NCAM-negative mice and correlate precisely with the level of NCAM erroneously devoid of polySia during development ). Thalamocortical and corticothalamic projections form a major part of the internal capsule and numerous studies deal with their formation (for examples, see Métin and Godement, 1996;Métin et al, 1997;Molnár and Cordery, 1999;Ma et al, 2002;Molnár et al, 2003;Andrews et al, 2006;Ló pez-Bendito et al, 2007;Wright et al, 2007;Demyanenko et al, 2010). As shown before, polySia is crucial for branch formation of thalamocortical axons within cortical layer 4 (Yamamoto et al, 2000).…”

Section: Introductionmentioning

confidence: 92%

Thalamocortical Pathfinding Defects Precede Degeneration of the Reticular Thalamic Nucleus in Polysialic Acid-Deficient Mice

Schiff¹,

Röckle²,

Burkhardt³

et al. 2011

J. Neurosci.

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IVϪ/Ϫ ) mice characterized by severe defects of major brain axon tracts, including internal capsule hypoplasia. Here, we demonstrate that misguidance of thalamocortical fibers and deficiencies of corticothalamic connections contribute to internal capsule defects in II Ϫ/Ϫ IV Ϫ/Ϫ mice. Thalamocortical fibers cross the primordium of the reticular thalamic nucleus (Rt) at embryonic day 14.5, before they fail to turn into the ventral telencephalon, thus deviating from their normal trajectory without passing through the internal capsule. At postnatal day 1, a reduction and massive disorganization of fibers traversing the Rt was observed, whereas terminal deoxynucleotidyl transferase dUTP nick end labeling and cleaved caspase-3 staining indicated abundant apoptotic cell death of Rt neurons at postnatal day 5. Furthermore, during postnatal development, the number of Rt neurons was drastically reduced in 4-week-old IIN Ϫ/Ϫ triple knock-out animals displaying no internal capsule defects. Thus, degeneration of the Rt in II Ϫ/Ϫ IV Ϫ/Ϫ mice may be a consequence of malformation of thalamocortical and corticothalamic fibers providing major excitatory input into the Rt. Indeed, apoptotic death of Rt neurons could be induced by lesioning corticothalamic fibers on whole-brain slice cultures. We therefore propose that anterograde transneuronal degeneration of the Rt in polysialylation-deficient, NCAM-positive mice is caused by defective afferent innervation attributable to thalamocortical pathfinding defects.

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Robo1 and Robo2 Cooperate to Control the Guidance of Major Axonal Tracts in the Mammalian Forebrain

Cited by 207 publications

References 50 publications

Molecular Mechanisms Controlling Midline Crossing by Precerebellar Neurons

Molecular Mechanisms Controlling Midline Crossing by Precerebellar Neurons

EphB receptor forward signaling regulates area-specific reciprocal thalamic and cortical axon pathfinding

Thalamocortical Pathfinding Defects Precede Degeneration of the Reticular Thalamic Nucleus in Polysialic Acid-Deficient Mice

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