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The Journal of Neuroscience, November 2, 2005, 25(44):10119-10130; doi:10.1523/JNEUROSCI.3455-05.2005

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Development/Plasticity/Repair
Molecular Control of Spinal Accessory Motor Neuron/Axon Development in the Mouse Spinal Cord

Allison K. Dillon,¹ Shinobu C. Fujita,³ Michael P. Matise,⁴ Andrew A. Jarjour,⁵ Timothy E. Kennedy,⁵ Heike Kollmus,⁶ Hans-Henning Arnold,⁶ Joshua A. Weiner,⁷ Joshua R. Sanes,⁸ and Zaven Kaprielian^1,2

Departments of ¹Neuroscience and ²Pathology, Albert Einstein College of Medicine, Bronx, New York 10461, ³Mitsubishi Kagaku Institute of Life Sciences, Tokyo 194-8511, Japan, ⁴Department of Neuroscience and Cell Biology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, ⁵Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada H3A 2B4, ⁶Department of Cell and Molecular Biology, University of Braunschweig, D-38106 Braunschweig, Germany, ⁷Department of Biological Sciences, University of Iowa, Iowa City, Iowa 52242, and ⁸Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138

Within the developing vertebrate spinal cord, motor neuron subtypes are distinguished by the settling positions of their cell bodies, patterns of gene expression, and the paths their axons follow to exit the CNS. The inclusive set of cues required to guide a given motor axon subtype from cell body to target has yet to be identified, in any species. This is attributable, in part, to the unavailability of markers that demarcate the complete trajectory followed by a specific class of spinal motor axons. Most spinal motor neurons extend axons out of the CNS through ventral exit points. In contrast, spinal accessory motor neurons (SACMNs) project dorsally directed axons through lateral exit points (LEPs), and these axons assemble into the spinal accessory nerve (SAN). Here we show that an antibody against BEN/ALCAM/SC1/DM-GRASP/MuSC selectively labels mouse SACMNs and can be used to trace the pathfinding of SACMN axons. We use this marker, together with a battery of transcription factor-deficient or guidance cue/receptor-deficient mice to identify molecules required for distinct stages of SACMN development. Specifically, we find that Gli2 is required for the initial extension of axons from SACMN cell bodies, and that netrin-1 and its receptor Dcc are required for the proper dorsal migration of these cells and the dorsally directed extension of SACMN axons toward the LEPs. Furthermore, in the absence of the transcription factor Nkx2.9, SACMN axons fail to exit the CNS. Together, these findings suggest molecular mechanisms that are likely to regulate key steps in SACMN development.

Key words: spinal accessory motor neurons; BEN/ALCAM/SC1/DM-GRASP/MuSC; Gli2; netrin; DCC; Nkx2.9; exit point

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Received June 14, 2005; revised September 14, 2005; accepted September 15, 2005.

This article has been cited by other articles:

				S. L. Reeber, N. Sakai, Y. Nakada, J. Dumas, K. Dobrenis, J. E. Johnson, and Z. Kaprielian Manipulating Robo Expression In Vivo Perturbs Commissural Axon Pathfinding in the Chick Spinal Cord J. Neurosci., August 27, 2008; 28(35): 8698 - 8708. [Abstract] [Full Text] [PDF]

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