UNC5C is required for spinal accessory motor neuron development.

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Animals, Critical-Period-(Psychology), Embryo, Female, Gene-Expression-Regulation-Enzymologic, Immunohistochemistry, In-Situ-Hybridization, Mice-Knockout, Motor-Neurons, Pregnancy, Receptors-Cell-Surface, Receptors-Nerve-Growth-Factor, Spinal-Cord

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Mol Cell Neurosci 2007 Jul; 35(3):482-9.


In both invertebrates and vertebrates, UNC5 receptors facilitate chemorepulsion away from a Netrin source. Unlike most motor neurons in the embryonic vertebrate spinal cord, spinal accessory motor neuron (SACMN) cell bodies and their axons translocate along a dorsally directed trajectory away from the floor plate/ventral midline and toward the lateral exit point (LEP). We have recently shown that Netrin-1 and DCC are required for the migration of SACMN cell bodies, in vivo. These observations raised the possibility that vertebrate UNC5 proteins mediate the presumed repulsion of SACMN away from the Netrin-rich ventral midline. Here, we show that SACMN are likely to express UNC5A and UNC5C. Whereas SACMN development proceeds normally in UNC5A null mice, many SACMN cell bodies fail to migrate away from the ventral midline and inappropriately cluster in the ventrolateral spinal cord of mouse embryos lacking UNC5C. These results support an important role for UNC5C in SACMN development.