| Title: |
Transient neuronal populations are required to guide callosal axons: a role for semaphorin 3C |
| Authors: |
Niquille, Mathieu; Garel, Sonia; Mann, Fanny; Hornung, Jean-Pierre; Otsmane, Belkacem; Chevalley, Sébastien; Parras, Carlos; Guillemot, Francois; Gaspar, Patricia; Yanagawa, Yuchio; Lebrand, Cécile |
| Contributors: |
Department of Cellular Biology and Morphology; Université de Lausanne = University of Lausanne (UNIL); Génétique moléculaire du développement; Département de Biologie - ENS-PSL (IBENS); École normale supérieure - Paris (ENS-PSL); Université Paris Sciences et Lettres (PSL)-Université Paris Sciences et Lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Paris (ENS-PSL); Université Paris Sciences et Lettres (PSL)-Université Paris Sciences et Lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM); Institut de Biologie du Développement de Marseille (IBDM); Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS); Division of Molecular Neurobiology; National Institute for Medical Research; Institut du Fer à Moulin; Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM); Department of Genetic and Behavioral Neuroscience; Gunma University Graduate School of Medicine; Solution Oriented Research for Science and Technology (SORST); Japan Science and Technology Agency; This work was supported by the institutional research funds of the DBCM and by the European Commission Coordination Action ENINET (contract number LSHM-CT-2005-19063). CL is funded by the FNS. SG is a recipient of the HFSPO Career Development Award, the EURYI award, and is funded by the ARC, FRC, and la Ville de Paris. FM is supported by the ANR young investigator program and funded by the FRC. SG and PG are supported by the INSERM. YY is funded by the Ministry of Education, Culture, Sports, Science, and Technology of Japan. |
| Source: |
ISSN: 1544-9173. |
| Publisher Information: |
CCSD; Public Library of Science |
| Publication Year: |
2009 |
| Collection: |
Aix-Marseille Université: HAL |
| Subject Terms: |
MESH: Acrocallosal Syndrome; MESH: Animals; MESH: Humans; MESH: Mice; MESH: Neural Pathways; MESH: Neurons; MESH: Neuropilin-1; MESH: Semaphorins; MESH: Axons; MESH: Cell Line; MESH: Cell Movement; MESH: Coculture Techniques; MESH: Corpus Callosum; [SDV.BC]Life Sciences [q-bio]/Cellular Biology |
| Description: |
International audience ; The corpus callosum (CC) is the main pathway responsible for interhemispheric communication. CC agenesis is associated with numerous human pathologies, suggesting that a range of developmental defects can result in abnormalities in this structure. Midline glial cells are known to play a role in CC development, but we here show that two transient populations of midline neurons also make major contributions to the formation of this commissure. We report that these two neuronal populations enter the CC midline prior to the arrival of callosal pioneer axons. Using a combination of mutant analysis and in vitro assays, we demonstrate that CC neurons are necessary for normal callosal axon navigation. They exert an attractive influence on callosal axons, in part via Semaphorin 3C and its receptor Neuropilin-1. By revealing a novel and essential role for these neuronal populations in the pathfinding of a major cerebral commissure, our study brings new perspectives to pathophysiological mechanisms altering CC formation. |
| Document Type: |
article in journal/newspaper |
| Language: |
English |
| Relation: |
info:eu-repo/semantics/altIdentifier/pmid/19859539; PUBMED: 19859539 |
| DOI: |
10.1371/journal.pbio.1000230 |
| Availability: |
https://inserm.hal.science/inserm-00707639; https://inserm.hal.science/inserm-00707639v1/document; https://inserm.hal.science/inserm-00707639v1/file/journal.pbio.1000230.pdf; https://doi.org/10.1371/journal.pbio.1000230 |
| Rights: |
https://about.hal.science/hal-authorisation-v1/ ; info:eu-repo/semantics/OpenAccess |
| Accession Number: |
edsbas.EF176057 |
| Database: |
BASE |