Close Homolog of L1 and Neuropilin 1 Mediate Guidance of Thalamocortical Axons at the Ventral Telencephalon
| Autor: | Melitta Schachner, Ashton W. Powell, Lilian Enriquez-Barreto, Amanda G. Wright, Franck Polleux, Galina P. Demyanenko, Patricia F. Maness, Tracy S. Tran |
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| Přispěvatelé: | National Institutes of Health (US), The Pew Charitable Trusts, National Institute of Neurological Disorders and Stroke (US), North Carolina State University, Ministerio de Educación y Ciencia (España) |
| Rok vydání: | 2007 |
| Předmět: |
Telencephalon
L1 family Growth Cones Somatosensory Mice Transgenic Biology Mice Thalamocortical Thalamus Semaphorin Cell adhesion molecule Neural Pathways Neuropilin 1 medicine Neuropilin Animals Axon Crosses Genetic Cerebrum Axon guidance General Neuroscience SEMA3A Articles Axons Mice Mutant Strains Neuropilin-1 Protein Structure Tertiary medicine.anatomical_structure nervous system Cell Adhesion Molecules Neuroscience |
| Zdroj: | The Journal of Neuroscience. 27:13667-13679 |
| ISSN: | 1529-2401 0270-6474 |
| DOI: | 10.1523/jneurosci.2888-07.2007 |
| Popis: | We report a cooperation between the neural adhesion molecule close homolog of L1 (CHL1) and the semaphorin 3A (Sema3A) receptor, neuropilin 1 (Npn1), important for establishment of area-specific thalamocortical projections. CHL1 deletion in mice selectively disrupted the projection of somatosensory thalamic axons from the ventrobasal (VB) nuclei, causing them to shift caudally and target the visual cortex. At the ventral telencephalon, an intermediate target with graded Sema3A expression, VB axons were caudally shifted in CHL1 − embryos and in Npn1Sema−/− mutants, in which axons are nonresponsive to Sema3A. CHL1 colocalized with Npn1 on thalamic axons, and associated with Npn1 through a sequence in the CHL1 Ig1 domain that was required for Sema3A-induced growth cone collapse. These results identify a novel function for CHL1 in thalamic axon responsiveness to ventral telencephalic cues, and demonstrate a role for CHL1 and Npn1 in establishment of proper targeting of specific thalamocortical projections. This work was supported by National Institutes of Health Grants NS049109 (P.F.M.) and MH064056 (Silvio Conte Center for Neuroscience of Mental Disorders), the Pew Charitable Trust (F.P.), March of Dimes (F.P.), and National Institute of Neurological Disorders and Stroke Center Grant P30NS0445892 to the University of North Carolina Neuroscience Center for support of the Confocal and Hybridization Facilities. L.E.-B. was supported by the Spanish Ministry of Education and Science. |
| Databáze: | OpenAIRE |
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