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The Journal of Neuroscience, December 12, 2007, 27(50):13667-13679; doi:10.1523/JNEUROSCI.2888-07.2007

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Cellular/Molecular
Close Homolog of L1 and Neuropilin 1 Mediate Guidance of Thalamocortical Axons at the Ventral Telencephalon

Amanda G. Wright,^1,2 Galina P. Demyanenko,^1,2 Ashton Powell,² Melitta Schachner,^3,4,5 Lilian Enriquez-Barreto,^1,2,7 Tracy S. Tran,⁶ Franck Polleux,² and Patricia F. Maness^1,2

¹Department of Biochemistry and ²Neuroscience Research Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599, ³Universitaet Hamburg, D-20246 Hamburg, Germany; ⁴New Jersey Professor of Spinal Cord Research, Keck Center for Collaborative Neuroscience, Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, New Jersey 08854, ⁵Sino-German Center for Neuroscience, Dalian Medical University, Dalian 116011, Liaoning Province, China, ⁶Department of Neuroscience, Howard Hughes Medical Institute, John Hopkins University School of Medicine, Baltimore, Maryland 21218, and ⁷Instituto de Neurociencias de Alicante, 03550 Alicante, Spain

Correspondence should be addressed to Patricia F. Maness at the above address. Email: srclab{at}med.unc.edu

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 Npn1^Sema–/– 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.

Key words: thalamocortical; axon guidance; cell adhesion molecule; semaphorin; neuropilin; somatosensory

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Received June 25, 2007; revised Aug. 21, 2007; accepted Sept. 12, 2007.

Correspondence should be addressed to Patricia F. Maness at the above address. Email: srclab{at}med.unc.edu

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